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Carmen Dell'Orefice made the special edition cover of New You magazine; the supermodel is 83 years old. Wearing all black, pearls and a classic pout, Dell'Orefice admitted she's still "figuring out how to do the job" as she confronts a territory businesses tend to avoid: age and white hair. With more magazine covers in the past 25 years than her whole 70-plus years of working in the industry, the supermodel says she feels she's taking a stand for age. The new issue of New You will hit newsstands on February 11.


text:
> source: [scss/parts/list](../../src/scss/parts/_list.scss)

## Usage

### list

Simply none-list-style list.

```html
<ul class="list">
  <li>item 1</li>
  <li>item 2</li>
  <li>item 3</li>
</ul>
```

### list-group

```html
<ul class="list-group">
  <li>item 1</li>
  <li>item 2</li>
  <li>item 3</li>
</ul>
```

### list-horizontal

```html
<ul class="list-horizontal">
  <li>item 1</li>
  <li>item 2</li>
  <li>item 3</li>
</ul>
```

### breadcrumb

default separator is "/".

```html
<ul class="breadcrumb">
  <li><a href="#">scss</a></li>
  <li><a href="#">parts</a></li>
  <li>list</li>
</ul>
```

## SCSS variables

``` scss
$list-border-width: 1px !default;
$list-border-color: $border-color !default;
$list-padding-y: .6em !default;
$list-padding-x: .3em !default;
$list-group-padding-y: .4em !default;
$list-group-padding-x: .8em !default;
$list-group-padding: .4em .8em !default;
$list-group-border-radius: $radius-normal !default;
$list-group-hover-bg-color: rgba($background-color-invert, .1) !default;
$list-group-active-bg-color: $primary-color !default;
$list-group-active-color: get-contrast($list-group-active-bg-color) !default;
$breadcrumb-separator: '/' !default;
$breadcrumb-space: .4em !default;
```

redpajama_set_name: RedPajamaGithub


text:
The role of PET in dementia diagnosis and treatment
By Lina Mehta, MD, and Smitha Thomas, MD, University Hospitals of Cleveland, Case Western Reserve University, Cleveland, OH
Dr. Mehta is an Associate Professor of Radiology, and Dr. Thomas is a Radiology Fellow, at the University Hospitals of Cleveland, Case Western Reserve University, Cleveland, OH.
Dementia is an acquired, progressive, global impairment of intellectual functioning involving memory, language, thinking, and perception. This disorder can be caused by more than 80 diseases, a few of which can be reversible. Dementia can present a diagnostic challenge to clinicians as there can be much overlap between the various causes (Table 1). In addition, several of the diseases share common histopathologic and clinical features, and rather than reflecting discrete entities, are felt to be part of a spectrum of neurodegenerative syndromes.1,2 Currently, 35 million people worldwide are affected by dementia, with 5 million new cases added every year. In the absence of new treatment breakthroughs, 80 million cases are predicted by 2040,3 with the rising prevalence due mainly to increasing life expectancy.
Criteria for dementia
The clinical diagnosis of dementia is based mainly on clinical criteria, such as those delineated in the DSM-IV and DSM-TR.4 The criteria will be revised this year, but currently they consist of the development of multiple cognitive deficits, including impairments in memory andin at least one of the following: language, motor activity, recognition, and executive function. In addition, the cognitive deficits must be severe enough to interfere with social/professional function, and they must represent a decrease from baseline.
A diagnosis of dementia should not be made if the cognitive deficits occur exclusively during the course of a delirium. However, dementia may be related etiologically to a general medical condition, cerebrovascular disease, persisting effects of substance abuse (including toxin exposure), infections like HIV, or multiple other etiologies. Alzheimer's disease (AD) is usually diagnosed by excluding the above etiologies; each of these is classified as a separate category in DSM-TR.
Neuronuclear imaging applications in dementia
Patients undergoing a dementia work-up must have a comprehensive clinical exam that includes a medical history obtained from both the patient and a well-acquainted informant, cognitive scales or neuropsychological testing, laboratory tests, and structural imaging, such as magnetic resonance imaging (MRI) and computed tomography (CT). Single photon emission computed tomography (SPECT) has historically been the modality of choice for functional neuroimaging in the dementia work up, but is being replaced by positron emission tomography (PET). SPECT mainly assesses perfusion, while PET focuses primarily on metabolism, with both presenting similar diagnostic information. The advantages of PET over SPECT include better spatial resolution and the ability to quantify changes. In addition, the magnitude of hypometabolism seen with 18FDG-PET is frequently greater than that seen with SPECT.5 Common tracers for SPECT imaging include the cerebral blood flow agents 99m-Tc hexamethylpropyleneamineoxime (HM-PAO) and technetium Tc-99m bicisate. F-18 fluorodeoxyglucose (FDG) is the most commonly used agent in PET imaging. As a glucose analogue, FDG reflects cerebral glucose metabolism(Figure 1). Other PET agents are being developed to assess more specific cellular and neurotransmitter activities; several are discussed later in this article.
Protocol standardization is important for consistent FDG brain-PET imaging. The brain-PET protocol in our department includes securing intravenous (IV) access 15 minutes prior to injection, which minimizes stress. In addition, to minimize activation of the visual cortex and other brain centers, patients are provided with a comfortable resting place in a stress-free, quiet, semi-dark environment during the radiopharmaceutical uptake phase. Sedation, if necessary, should be performed after radiopharmaceutical dosing. The scan itself is performed in a comfortable but standardized position with contemporaneous acquisition of low-dose CT images for attenuation correction. Postprocessed images are digitally coregistered and reconstructed in the orthogonal planes for interpretation. The software used in our department also allows for digital coregistration with MRI.
Alzheimer's disease (AD)
AD, the most common form of dementia, was originally described in 1907 by the German psychiatrist and neuropathologist, Alois Alzheimer, who presented clinical and neuropathological features of a demented woman who died at age 51. Alzheimer noted postmortem pathology findings of thinned cerebral cortex, senile plaques, and neurofibrillary tangles (Figure 2), which are still considered to be pathologic hallmarks of the disease. AD is estimated to cause approximately 70% of all dementias. The age of onset is typically between 40 and 90 years,with greater incidence in those ≥65 years of age. The prevalence of the disease rises exponentially with age, increasing from 3% in those aged50-75 years to 50% among those ≥80 years old.6 The risk factors for AD are summarized in Table 2.
AD is a major health problem, bringing enormous economic, social, and personal costs. Data from the National Institute of Aging, a division of the U.S. National Institutes of Health, indicate that 5.1 million Americans currently have AD and the cost of care approaches $148 billion per year. Based on its current incidence, the aging of baby boomers, and the absence of effective prevention, an estimated 72 million people will be affected with AD in 2030.7
Disease spectrum
AD is a progressive neurodegenerative disease that results in irreversible loss of brain cells. The disease usually begins with mild memory problems and ends with severe brain damage, severe memory loss, confusion, depression, hallucinations, delusions, restlessness, sleeplessness,and loss of appetite. The most common and distinctive hallmark histologic brain lesions are senile plaques and neurofibrillary tangles (NFTs).The disease is felt to represent a spectrum that extends from mild cognitive impairment (MCI) to severe AD. In MCI, patients demonstrate decreased memory or language that is severe enough to be noticeable but not severe enough to interfere with daily life; it is seen in up to 20% ofAmericans and has 2 subtypes — nonamnesiac and amnesiac. Patients in the nonamnesiac category present with behavioral changes, including alterations in language, judgment, and attention. Patients with the amnesiac variety are often aware of memory issues and are still able to function effectively. Not all patients with MCI will progress to AD; annually, 10% to 15% of patients with amnesiac MCI will progress, while others may improve with time. PET imaging can help with early identification and interventions in those who may progress.8 Standardized primary cognitive assessments, such as the mini-mental state examination (MMSE), provide a brief, focused survey of cognitive domains most often affected in AD and allow for objective documentation of cognitive dysfunction.
Role of PET in the diagnosis of AD
Brain imaging with MRI, SPECT, and PET can improve diagnostic accuracy in differentiating AD from potentially treatable causes of dementia such as toxic metabolic states, depression, and normal pressure hydrocephalus. When PET results are combined with clinical criteria, the false positive rate in AD can be reduced from 23% to 11%.9 The classic pattern of AD on PET imaging is bilateral temporoparietal and posterior cingulate cortex hypometabolism (Figures 3 and 4); abnormal metabolism can also be seen asymmetrically, particularl yearly in the disease. Frontal lobe involvement may also be seen in later stages (Figure 5). The exact cause for the decline in brain glucose metabolism in AD remains unclear. Hippocampal atrophy may be seen on conventional cross-sectional imaging.10,11 Hoffman et al showed that FDG-PET demonstration of the classic metabolic abnormality in patients with pathologically verified AD has a sensitivity of 93%, a specificity of 63%, and an accuracy of 82%.10 Sparing of primary neocortical areas, including the sensorimotor cortex, visual cortex, subcortical gray matter, basal ganglia, thalami, and cerebellum could help differentiate AD from subcortical causes of dementia like Parkinson's dementia, vascular dementia, etc. FDG-PET imaging can also help evaluate MCI. A large multicenter study showed that MCI patients demonstrated primarily posterior cingulate cortex and hippocampal hypometabolism (81%); neocortical abnormalities varied according to neuropsychological profiles.A classical AD metabolic pattern was observed in 79% of MCI patients who presented with deficits in multiple cognitive domains and in 31% of patients with amnesic MCI. FDG-PET abnormalities in nonamnesiac MCI ranged from normal metabolism to patterns resembling frontotemporal dementia and diffuse Lewy body disease, suggesting another dimension to the spectrum of AD.12 Preliminary PET data show a promising ability to predict progression from MCI to AD. Landau et al evaluated multiple markers for disease progression and, among their findings, noted that patients with abnormal results on FDG-PET and with abnormal episodic memory were 11.7 times more likely to convert from MCI to AD.13
A meta-analysis of 15 articles published between 1989 and 2003 demonstrated a sensitivity of 86% (95% confidence interval [CI]:76%, 93%) and a specificity of 86% (95% CI: 72%, 93%) for FDG PET14 in the diagnosis of AD. However, recent studies on larger patient populations demonstrate sensitivities approaching 93% to 95% in AD12,15 (Table 3). Early and accurate AD diagnosis is important for patients to derive the maximum benefit from available pharmacologic and cognitive therapies. Although no definitive treatment orcure is available for AD at this time, different pharmacologic agents are being actively investigated; several are available to treat symptoms of the disease. Cholinesterase inhibitors like Aricept, the most widely used and only FDA-approved drug for all stages of AD, improves acetylcholine levels, which are deficient in all stages of the disease. Available data suggest that approximately 15% to 40% of AD patients treated with the drug show varying degrees of cognitive improvement. Another drug, Namenda, approved for moderate-to-severe AD, is thought to regulate glutamate, a neuroprotective agent, which can reduce oxidative stress. Early diagnosis of AD also allows for contemporaneous initiation of palliative, psychosocial, and cognitive therapies, as well as initiation of support systems. It also provides the patient adequate time to address personal, financial, and legal ramifications of the disease.
Silverman et al performed a decision analysis to compare the relative value of a conventional approach (based on clinical criteria for the presence of dementia and excluding nonAD etiologies that could contribute to patients' symptoms) versus an FDG-PET-based strategy.16 The PET algorithm reduced false-negative and false-positive findings compared to the conventional clinical approach (3.1% vs. 82%, and12% vs. 23%, respectively, at a prevalence rate of 51.6% in the group). A cost saving of $1,138 per correct diagnosis and a lower cost-per-unit benefit were maintained over a wide range of tested values for sensitivity, specificity, cost of PET, and long-term care. Silverman concluded that using PET in the work-up of early dementia in elderly patients can contribute significantly and economically to the evaluation and treatment of these patients. The Center for Medicare and Medicaid Services (CMS), in a decision memorandum on Sept.15, 2004, ruledthat FDG brain-PET scans are reasonable and necessary in patients with a recently established diagnosis of dementia with cognitive decline documented for at least 6 months. Eligible patients are to have met the criteria for both AD and/or frontotemporal dementia (FTD) and to have already been evaluated for specific alternative degenerative diseases or causative factors. Medicare also covers FDG-PET in CMS approved practical clinical trials that focus on the utility of FDG-PET in the diagnosis or treatment of mild cognitive impairment or early dementia.17
FDG-PET has been shown to provide important prognostic information in dementia. A negative PET scan is indicative of unlikely progression of cognitive impairment for a mean follow-up of 3 years in those patients who initially present with cognitive symptoms of dementia.18
Diffuse Lewy body disease (DLB)
DLB is the second most common cause of dementia, accounting for 15% to 20% of all cases. Fluctuating cognition, visual hallucinations, and lowered attention span often precede memory loss; this contrasts with AD, in which prominent and progressive memory loss often precedes neuropsychiatric features. Patients with DLB may also demonstrate Parkinsonian-like symptoms. The specificity for diagnosis based on clinical criteria is variable (30% to 100%); sensitivity is low (22% to 75%).19 The pattern of FDG metabolism in DLB differs fromAD; in contrast to the classic appearance of bilateral temporal-parietal reductions in FDG metabolism with AD, DLB commonly appears as globally reduced cortical metabolism, most notably in the visual association cortex of the occipital lobe (Figure 6). The reduction in occipital glucose metabolism in DLB can differentiate DLB from AD with a sensitivity of 86% to 90% and a specificity of 80% to 91%.19,20 The reason for the selective involvement of the occipital region is unclear and has been attributed to the degeneration of dopaminergic neurons or cholinergic neurons from the basal nucleus of Meynert; imaging with dopaminergic ligands has been suggested to increase specificity for diagnosis of the disease. In addition, the relative preservation of the mid- or posterior-cingulate gyrus metabolism (cingulate island sign) may enhance PET specificity in differentiating DLB from AD.
A neurological movement disorder originally described in 1817 by James Parkinson, Parkinson's disease (PD) is characterized by the deterioration of neurons in the substantia nigra, resulting in decreased dopamine levels. Cognitive deficits appear in the late stage of the disease in about 41% of the patients with PD; these may range from isolated cognitive impairment to severe dementia. Imaging features of the disease often correlate with an AD-type pattern on functional FDG-PET imaging, although more occipital involvement and more sparing of the mesiotemporal area may be seen with PD. A recent study suggests that more extensive changes may actually be seen in PD patients with dementia;21 this study compared 18-FDG and 11-C PIB metabolic patterns along with structural changes on MRI in nondemented Parkinson's (PD) and demented Parkinson's (PDD) patients, with healthy patients serving as controls. Their data suggest that the development of dementia in PD may also be associated with frontal lobe atrophy on MRI, with extension of hypometabolism on FDG-PET beyond the occipital lobe into the frontal lobe, and even through more diffuse brain areas, such as the deep brain structures. The degree of glucose hypometabolism was associated with the degree of cognitive impairment. Beta amyloid deposition is not believed to be a hallmark of PD dementia; if seen postmortem, its presence is thought to reflect the coincidental development of Alzheimer's disease.
Frontotemporal lobar dementia (FTD)
FTD is a general term for a diverse group of disorders associated with selective degeneration of the prefrontal and anterior temporal cortex. Given the distribution of the cortical abnormalities, salient clinical characteristics of these disorders include profound alterations in personality and social conduct, agnosia, and impulsivity. These symptoms occur in the context of relative preservation of the instrumental functions of perception,spatial skills, praxis, and memory.22
Pick's disease accounts for the largest proportion (at least 70%) of patients with frontotemporal lobar degeneration; the disease is characterized by the presence of Pick bodies, protein tangles in neuronal tissues. Disease onset tends to occur at a younger age than that of AD,with the most common incidence occurring between ages 45 and 65; the disorder can also present before age 30, as well as in the elderly.The cause of Pick's disease is unknown; some forms of inherited frontal lobe dementia can be indistinguishable, clinically and histologically, from Pick's disease.
Differentiating between FTD and AD is currently based on clinical data and examination, but the distinct metabolic patterns of both diseases as seen on PET can significantly improve diagnostic accuracy. A prospective FDG-PET study evaluated 22 patients with FTD who underwent both baseline and follow-up scans during an average duration of 19.5 months. PET demonstrated symmetrical hypometabolism of the frontal lobes with relative sparing of the motor cortex, caudate nuclei, insula, and thalami at baseline.23 At follow-up, further significant reductions in glucose metabolism were observed in the parietal and temporal cortices. The use of FDG-PET stereotactic surface projection (SSP) metabolic and statistical maps have been shown to improve sensitivity of PET in early diagnosis of FTD.20 Preliminary data from neurochemical studies of FTD patients, as well as functional PET imaging using serotonin receptors, have indicated abnormalities in serotonin metabolism, which has led to clinical trials of drugs with serotoninergic effects.
Newer radiopharmaceuticals
In the past few years, much attention has focused on the development of radiotracers for PET imaging of more specific pathologic processes, including agents that detect the beta-amyloid deposits, the neurofibrillary tangles, and other processes in AD. The deposition of beta-amyloid (Aβ) is thought by many to be an early event in the pathogenesis of AD. Pittsburgh Compound B (C11PIB), a thioflavine analogue, was the first tracer used to selectively label Aβ in vivo. A relatively simple and practical way to quantify Aβ uptake in vivo in a clinical setting is by quantifying C11PIB binding. In AD, marked PIB retention occurs in areas of ß-amyloid deposition, such as in the temporoparietal cortex. Recent studies indicate a future potential use for C11PIB in predicting time of progression of MCI to AD.24 Cholinergic agents are also being developed for PET imaging and may provide additional evidence for the cholinergic hypothesis of AD, as well as provide insight into the functional mechanisms of novel drug therapies directed to the cholinergic system.
The evaluation of dopamine receptor integrity with carbon-11 dihydrotetrabenazine (DTBZ) has also been extensively researched in patients with diffuse Lewy body disease and Parkinson's disease. Early studies suggest that the distribution volume of DTBZ is significantly decreased in the caudate nuclei and putamen in DLB and PD patients compared to patients with AD.25 Several other agents are in the pipeline for targeted receptor imaging, several of which are mentioned in Table 4.
The role of PET in the clinical workup and management of dementia is expected to increase in the near future, not only for preclinical and differential diagnoses but also for the evaluation of response to novel therapies that are currently in development. The widespread availability ofPET scanners, along with new and improved quantitative analysis methods, has improved scan quality and diagnostic information provided by these studies. Data suggest that including PET in the diagnostic algorithm of patients with dementia can result in more cost-effective and accurate diagnoses, particularly in differentiating DD from FTD.
Kertesz A. Pick Complex: An integrative approach to frontotemporal dementia: Primary progressive aphasia, corticobasal degeneration, and progressive supranuclear palsy. Neurologist. 2003;9:311-317.
Kertesz A, Hudson L, Mackenzie IR, Munoz DG. The pathology and nosology of primary progressive aphasia. Neurology. 1994;44:2065-2072.
Ferri CP, Prince M, Brayne C, et al. Global prevalence of dementia: A Delphi consensus study. Lancet. 2005;366:2112-2117.
DSM-IV-TR: The Current Manual. http://www.psych.org/MainMenu/Research/DSMIV/DSMIVTR.aspx. Accessed January 13, 2011.
Silverman DH. Brain 18F-FDG PET in the diagnosis of neurodegenerative dementias: Comparison with perfusion SPECT and with clinical evaluations lacking nuclear imaging. J Nucl Med. 2004;45:594-607.
Zhu CW, Sano M. Economic considerations in the management of Alzheimer's disease. Clin Interv Aging. 2006;1:143-154.
General Information. http://www.nia.nih.gov/Alzheimers/AlzheimersInformation/GeneralInfo/. Accessed January 13, 2011.
Schuff N, Zhu XP. Imaging of mild cognitive impairment and early dementia. Br J Radiol. 2007;80 Spec No 2:S109-14.
Silverman DH, Cummings JL, Small GW, et al. Added clinical benefit of incorporating 2-deoxy-2-[18F]fluoro-D-glucose with positron emission tomography into the clinical evaluation of patients with cognitive impairment. Mol Imaging Biol. 2002;4:283-293.
Hoffman JM, Welsh-Bohmer KA, Hanson M, et al. FDG PET imaging in patients with pathologically verified dementia. J Nucl Med. 2000;41: 1920-1928.
Yamaguchi S, Meguro K, Itoh M, et al. Decreased cortical glucose metabolism correlates with hippocampal atrophy in Alzheimer's disease as shown by MRI and PET. J Neurol Neurosurg Psychiatry. 1997;62:596-600.
Mosconi L, Tsui WH, Herholz K, et al. Multicenter standardized 18F-FDG PET diagnosis of mild cognitive impairment, Alzheimer's disease, and other dementias. J Nucl Med. 2008;49:390-398.
Landau SM, Harvey D, Madison CM, et al. Comparing predictors of conversion and decline in mild cognitive impairment. Neurology. 2010;75:230-238.
Patwardhan MB, McCrory DC, Matchar DB, et al. Alzheimer disease: Operating characteristics of PET--a meta-analysis. Radiology. 2004;231:73-80.
Morinaga A, Ono K, Ikeda T, et al. A comparison of the diagnostic sensitivity of MRI, CBF-SPECT, FDG-PET and cerebrospinal fluid biomarkers for detecting Alzheimer's disease in a memory clinic. Dement Geriatr Cogn Disord. 2010;30:285-292.
Silverman DH, Gambhir SS, Huang HW, et al. Evaluating early dementia with and without assessment of regional cerebral metabolism by PET: A comparison of predicted costs and benefits. J Nucl Med. 2002;43:253-266.
Centers for Medicare & Medicaid Services. http://www.cms.gov/mcd/viewncd.asp?ncd_id=220.6.13&ncd_version=2&basket=ncd:220.6.13:2:PET+(FDG)+for+Dementia+and+Neurodegenerative+Diseases. Accessed January 13, 2011.
Silverman DH, Small GW, Chang CY, et al. Positron emission tomography in evaluation of dementia: Regional brain metabolism and long-term outcome. JAMA. 2001;286:2120-2127.
Lim SM, Katsifis A, Villemagne VL, et al. The 18F-FDG PET cingulate island sign and comparison to 123I-beta-CIT SPECT for diagnosis of dementia with Lewy bodies. J Nucl Med. 2009;50:1638-1645.
Minoshima S, Foster NL, Sima AA, et al. Alzheimer's disease versus dementia with Lewy bodies: Cerebral metabolic distinction with autopsy confirmation. Ann Neurol. 2001;50:358-365.
Jokinen P, Scheinin N, Aalto S, et al. [(11)C]PIB-, [(18)F]FDG-PET and MRI imaging in patients with Parkinson's disease with and without dementia. Parkinsonism Relat Disord. 2010;16:666-670.
Neary D, Snowden J, Mann D. Frontotemporal dementia. Lancet Neurol. 2005;4:771-780.
Diehl-Schmid J, Grimmer T, Drzezga A, et al. Decline of cerebral glucose metabolism in frontotemporal dementia: A longitudinal 18F-FDG-PET-study. Neurobiol Aging. 2007;28: 42-50.
Jack CR,Jr, Wiste HJ, Vemuri P, et al. Brain beta-amyloid measures and magnetic resonance imaging atrophy both predict time-to-progression from mild cognitive impairment to Alzheimer's disease. Brain. 2010;133:3336-3348.
Koeppe RA, Gilman S, Junck L, et al. Differentiating Alzheimer's disease from dementia with Lewy bodies and Parkinson's disease with (+)-[11C] dihydrotetrabenazine positron emission tomography. Alzheimers Dement. 2008;4(1 Suppl 1):S67-76.
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2020 May bank holiday will be moved to mark 75th anniversary of VE Day
Source: Department for Business Enterprise and Regulatory Reform | | 19/06/2019
The government has announced that the date of next year's early May bank holiday is to move from Monday, 4 May to Friday, 8 May to mark the 75th anniversary of VE Day. This is only the second time ever that the early May bank holiday has been moved – the first was in 1995 to mark the 50th anniversary of VE Day. There will be commemorative events taking place across the country over the three-day weekend to honour the sacrifice made by men and women during the Second World War. VE Day was first celebrated on 8 May 1945 when Allied Forces formally accepted Germany's surrender.
The early May bank holiday will move in England, Wales and Northern Ireland, where it is achieved by a Royal Proclamation made under the Banking and Financial Dealings Act 1971. Bank holidays are a devolved issue in Scotland. However, Scottish Ministers have also confirmed the change of date on the Scottish government's website.
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Our Dyn Concierge team handled nearly 15,000 phone calls and 75,000 tickets in 2011. That doesn't even count assisting our sales team, who have the Implementation team running around non-stop all day assisting our new DNS and Email customers.
However, our team isn't nearly as big as you would think when you first look at those numbers. We come from a variety of backgrounds, ranging from IT, public sector, military, retail, special education, TV industry and more. With all that diversity, there is one simple constant on how we can learn our job, do our job, and do it so well: repetition and refinement.
When I first came to Dyn back in April 2009, I was immediately warned that I would have a pop quiz occur quite often: "What is a MX record?" It was the inside joke of the Client Services team to see how fast a new person learns and how quickly they can react to an unexpected question at the most awkward of moments (mine was being asked in the restroom).
Every single new teammate has a moment about two to three weeks into the job that we have labeled "The Freak Out." They worry that they are not understanding the theory, the jargon, the scenarios and the gotchas and wonder if this is really the job for them.
This happens despite the entire team telling them non-stop how great they are doing. Still, they just don't believe it.
The light bulb goes on. You exhale. A smile appears on your face and you realize you are going to make it.
This repetition is key for the development of our Concierge and Implementation teams. This was not just true for the MX record question, but for just about every customer inquiry we come across. The key to surviving the training is repetition and refinement of our responses to our customers, whether they are external (our paying customers) or internal (our sales team). A member of the Concierge team will do thousands of calls and tickets over the course of a year, while our Implementation team will be on hundreds of sales calls a year and even more emails.
We will encounter just about every situation that can come up in DNS and Email. Yet in the end, every single scenario relies on the same basic set of principles for DNS and Email. When all else fails, you break down the issue, start from the basics and verify the several steps that have to happen for the service to work. The cause of the problem is quickly found and resolved. What results from this process is something quite remarkable.
Every single individual on the team has their own style, their own written responses and their own methods for assisting our customers with getting the answer to their question or fixing their issue.
We don't use scripts, because we want our team members to have their own identity and to show how knowledgeable and adaptable they really are. Every time you talk to us on the phone or correspond via email, you have a real smart human on the other end that simply knows their stuff, because of the repetition and refinement they underwent to provide world class customer service.
Chris Gonyea is a solutions architect at Oracle Dyn, a pioneer in managed DNS and a leader in cloud-based infrastructure that connects users with digital content and experiences across a global internet.


Find out how this Harvard grad who dropped his six-figure job made his way into becoming one of the most watched travel vloggers in Facebook.
Born from a middle-class Israeli-Palestinian family, Nuseir Yassin never imagined spending his college years in Harvard and becoming one of the most known travel vloggers in Facebook.
In his creations, he described himself as timid and socially awkward, coming from a modest family, according to Business Insider. His mother and father were respectively a teacher and psychologist who strived to provide their four children with quality education.
Despite the modesty of his lifestyle and status, Yassin did not feel constrained to map out his dreams within Israel. Ambitiously, he aimed to study in Ivy League colleges and universities. As such, he applied for Harvard where he was offered a scholarship for a degree in aerospace engineering. However, he majored in economics and eventually graduated.
After Harvard, Yassin jumped into the jungles of New York City, where he started out with a salary of at least $100,000 per annum to code for Venmo, a money transferring platform that Paypal owns. But despite getting a high-paying job, which is a fairly difficult achievement for a fresh graduate, Yassin got worn out. He felt that so much of his time was being wasted—time which he could have used to travel the world and dispel that feeling of tiredness.
"My job was overpaid. It wasn't satisfying enough," Yassin was quoted.
So with a $60,000 savings, Yassin quit his job after a year and a half and started to dedicate his life to traveling and documenting his journeys.
He first set eyes on destinations that were not much given attention by tourists. These include Rwanda, Tanzania, and Malta, among others. Since then, he has been geared toward presenting the online realm with a look of the world's underrated nooks that can equally offer so much wonder.
He shows the world a glimpse of these places through clips that span a minute in length, a period which can successfully narrate the lives of the people he encounters throughout his travels.
"I make videos about people's stories in a way that is human," Yassin said. "We live very busy lives. But everyone has a spare minute," he added.
Through his Facebook page titled Nas Daily, with "Nas" derived from the Arabic term for "people," Yassin is able to touch his growing followers—now over 6.3 million—with the inspiring stories he lives for. As such, Yassin has been driven to produce one video per day of his 1,000 days of traveling, of which more than 75 percent has been accomplished after at least 65 travel destinations.
Succeeding through his own effort in the social media marketing space, Yassin took on a career of consulting businesses and people who scout experts to produce multimedia content for them. Aside from the gains from his consultancy services, Yassin's main revenue source is Facebook ads on his videos, and he says his net worth is below the earnings of other travel vloggers as he estimates it to be at $250,000.
As for life beyond traveling, Yassin hopes to share his learnings to a set of potential vloggers from productions he plans to own a stake as part of the exchange for his lessons.


text:
Information on EC 2.7.11.17 - Ca2+/calmodulin-dependent protein kinase
for references in articles please use BRENDA:EC2.7.11.17
2 Transferases
2.7 Transferring phosphorus-containing groups
2.7.11 Protein-serine/threonine kinases
2.7.11.17 Ca2+/calmodulin-dependent protein kinase
Requires calmodulin and Ca2+ for activity. A wide range of proteins can act as acceptor, including vimentin, synapsin, glycogen synthase, myosin light chains and the microtubule-associated tau protein. Not identical with EC 2.7.11.18 (myosin-light-chain kinase) or EC 2.7.11.26 (tau-protein kinase).
All organisms Acropora Acropora digitifera Actina Actinobacteria Adeno-associated virus Aedes aegypti Aeschynomene evenia African swine fever virus Allium sativum Alphaproteobacteria Amoeba proteus Anaerolineae Anas platyrhynchos Anemonia sulcata animal Anser Apis mellifera Aplysia Aplysia californica Apoidea Apteronotus leptorhynchus Apus apus Arabidopsis Arabidopsis thaliana Arachis Areas Argynnis pandora Armoracia rusticana Asbestopluma hypogea Ascaris suum Ascomycota Aspergillus nidulans Avena sativa Avian sarcoma virus Babiana striata Bacopa monnieri Bacteria Blastocladiella emersonii Blattella germanica Bombus impatiens Bombus terrestris Bombyx Bombyx mori Bos taurus Boswellia Boswellia sacra Bovine rotavirus Brassica napus subsp. rapifera Caedius marinus Caenorhabditis elegans Caliadurgus cinereus Calyx Camellia sinensis Candida albicans Candida albicans BWP17 Candida dubliniensis Canis lupus familiaris Cannabis sativa Capra hircus Capsicum annuum Capsicum frutescens Carassius auratus Carthamus tinctorius Castor Casuarina glauca Cavia Cavia porcellus Chimaera Chironomus thummi Chiroptera Chlamydia pneumoniae Chlorophyta Chondrichthyes Citrus Citrus medica clinical samples Clostridia Clostridium Clostridium tyrobutyricum Clunio marinus Coffea racemosa Colletotrichum gloeosporioides Comamonadaceae Coprinopsis cinerea Cordyceps militaris Cricetinae Cricetulus griseus Cucumber mosaic virus Curcuma longa Cuscuta australis Cyclops Cynopterus sphinx Cytomegalovirus Danio rerio Decodes Dengue virus Desulfovibrio desulfuricans Dictyostelium Dictyostelium discoideum Digitalis Dione Diptera Doryteuthis pealeii Drosophila Drosophila C virus Drosophila melanogaster Eimeria Eisenia Eisenia fetida Electrophorus electricus Embryophyta Enterovirus A71 Epicoccum Equus caballus Escherichia Escherichia coli Euhadra eukaryota Eurosta solidaginis fabids Fallopia multiflora Felis catus Frankia Funaria hygrometrica Fungi Fusarium oxysporum Gallus gallus Ganoderma lucidum Gerbillinae Glycine max Glycine soja H1N1 subtype Hedysarum polybotrys Helicobacter pylori Hepacivirus C Hexapoda Hippocampus Homo sapiens Human alphaherpesvirus 1 Human betaherpesvirus 5 Human gammaherpesvirus 4 Human gammaherpesvirus 8 Human immunodeficiency virus 1 Indicator Ipomoea batatas Lamiinae Lamina Lateolabrax japonicus Lentivirus Lepidoptera Limulus Lobster Lotus Lotus japonicus Lymnaea Macaca Macaca mulatta Macaca mulatta polyomavirus 1 Macrobrachium nipponense Magnaporthe Magnoliophyta Mallotus Malus domestica Mammalia Manduca sexta Measles morbillivirus Mecolaesthus longissimus Medicago sativa Medicago truncatula Melanina Meleagris gallopavo Mesorhizobium loti Metaphire sieboldi Metarhizium anisopliae Metazoa Modiolus Mus musculus Mus musculus C57/Bl Mus musculus C57BL/6 Mus sp. Mustela putorius furo Naja atra Nannizzia gypsea Nelumbo nucifera Nematoda Neurospora Neurospora crassa Neurospora crassa ATCC 24698 Nicotiana attenuata Nicotiana benthamiana Nicotiana tabacum Ochetophila trinervis Odontaster validus Oriens Oryctolagus cuniculus Oryza sativa Ovis aries Oxalobacteraceae Pagothenia borchgrevinki Panax ginseng Panulirus interruptus Parasponia Parastagonospora nodorum Pealius liquidambari Periplaneta americana Phleum pratense Physarum Physarum polycephalum Physarum polycephalum Ng-1 Physcomitrella patens Pisum sativum plant Plasmodium Plasmodium berghei Plasmodium falciparum Plasmodium gallinaceum Platyrrhini Porcine circovirus 2 Porphyromonas gingivalis prawn Primates prion Proboscis Proteobacteria Prunus Pyricularia oryzae Rattus Rattus norvegicus Rheum rhabarbarum Rhizobiales Rhizophagus irregularis Rodentia Rotavirus Rous sarcoma virus Saccharomyces cerevisiae Salma Sarcophaga bullata Schistosoma japonicum Schizosaccharomyces pombe Sesbania rostrata Silvetia compressa Simian immunodeficiency virus Solanum lycopersicum Sphingomonadales Sphinx Sporothrix schenckii Staphylococcus aureus Staphylococcus aureus V8 Strawberry crinkle virus Streptococcus Streptomyces Strigiformes Suberites domuncula Suidae Sus scrofa Taenia Taraxacum officinale Tephritidae Tipula iridescent virus tobacco mosaic virus Torpedo Toxoplasma gondii Trachea Trematomus bernacchii Triticum aestivum Trypanosoma cruzi Tyto alba Tytonidae Ursidae Veillonella parvula Venus vertebrata vesicular stomatitis virus Viruses Vitis vinifera Xenopus Xenopus laevis Xenopus sp. yeasts Zea mays Ziziphus
Word Map
hippocampal
camks
autophosphorylation
postsynaptic
ca2+-dependent
nmda
dendritic
n-methyl-d-aspartate
cytoskeletal
calponin
calcium-dependent
calcineurin
excitatory
gizzard
signal-regulated
actomyosin
calmodulin-binding
phosphopeptide
activity-dependent
element-binding
actin-binding
amp-activated
l-type
desmin
glutamatergic
cam-binding
phospholamban
presynaptic
ca2+-calmodulin
nonmuscle
amp-dependent
autoinhibitory
actin-myosin
ca2+-calmodulin-dependent
actin-activated
calmidazolium
mgatpase
ampars
myosin-binding
p-creb
meromyosin
The enzyme appears in viruses and cellular organisms
a protein
a phosphoprotein
caldesmon, cam kinase ii, cam kinase, camkiv, calmodulin-dependent protein kinase, calcium/calmodulin-dependent protein kinase ii, camk ii, calcium/calmodulin-dependent protein kinase, camkiialpha, camkk, more
ACMPK
Aspergillus nidulans
alpha Ca2+/calmodulin-dependent protein kinase II
isoform alpha
alpha-Ca2+/calmodulin-dependent protein kinase II
Mus musculus
alpha-calcium/calmodulin-dependent protein kinase II
Rattus norvegicus
alpha-CaMK-II
alphaCa2+/CaM-dependent protein kinase II
alphaCaMKI
alphaCaMKII
beta Ca2+/calmodulin-dependent protein kinase II
isoform beta
Ca/CaM-dependent kinase-1
Ca2+-CaM-dependent protein kinase II
Ca2+/calmodulin-dependent kinase II
Ca2+/calmodulin-dependent kinase IIdelta
Q6PHZ2
Ca2+/calmodulin-dependent membrane-associated kinase
Ca2+/calmodulin-dependent protein kinase
Ca2+/calmodulin-dependent protein kinase 2
Q6AX64, Q91549, Q9DG00, Q9DG02
Ca2+/calmodulin-dependent protein kinase Ialpha
Ca2+/calmodulin-dependent protein kinase Igamma
Q7TNJ7
Ca2+/calmodulin-dependent protein kinase II
Ca2+/calmodulin-dependent protein kinase IIalpha
Ca2+/calmodulin-dependent protein kinase IIdelta
Ca2+/calmodulin-dependent protein kinase IIgamma
Ca2+/calmodulin-dependent protein kinase IV
Danio rerio
Q568I9
Ca2+/calmodulin-dependent protein kinase kinase
Ca2+/calmodulin-dependent protein kinase type IG
Ca2+/calmodulin-stimulated protein kinase II
Ca2+/CaM kinase II gamma G2
Ca2+/CaM-dependent protein kinase
Ca2+/CaM-dependent protein kinase II
Cavia porcellus
Ca2+/CaM-dependent protein kinase IIalpha
Ca2+/CaMK
Ca2+/CaMPK
calcium- and calmodulin-dependent kinase Ialpha
calcium-calmodulin dependent protein kinase IV
calcium-calmodulin-dependent protein kinase II
calcium-dependent protein kinase
calcium-independent calcium/calmodulin-dependent protein kinase II
calcium/calmodulin dependent protein kinase II
calcium/calmodulin dependent protein kinase II-alpha
calcium/calmodulin-dependent kinase
calcium/calmodulin-dependent kinase I
calcium/calmodulin-dependent protein kinase
calcium/calmodulin-dependent protein kinase 1G
calcium/calmodulin-dependent protein kinase I
calcium/calmodulin-dependent protein kinase Ialpha
Q8AYR3
calcium/calmodulin-dependent protein kinase II
calcium/calmodulin-dependent protein kinase II delta
calcium/calmodulin-dependent protein kinase II-alpha
calcium/calmodulin-dependent protein kinase IIalpha
calcium/calmodulin-dependent protein kinase IIbeta
calcium/calmodulin-dependent protein kinase IV
calcium/calmodulin-dependent protein kinase IV/protein serine/threonine phosphatase 2A signaling complex
calcium/calmodulin-dependent protein kinase type 2
calcium/calmodulin-dependent protein kinase type I
calcium/calmodulin-dependent protein kinase type II alpha chain
calcium/calmodulin-dependent protein kinase type II beta chain
calcium/calmodulin-dependent protein kinase type II delta chain
calcium/calmodulin-dependent protein kinase type II gamma chain
calcium/calmodulin-dependent protein kinase type IV catalytic chain
calcium/calmodulin-dependent serine protein kinase
calcium/calmodulin-dependent serine/threonine-protein kinase
caldesmon
calmodulin kinase I
calmodulin kinase IV
calmodulin-dependent protein kinase
calmodulin-dependent protein kinase IV
Calspermin
CaM kinase
CaM kinase Gr
CaM kinase IG
CaM kinase II
CaM kinase IIalpha
CAM kinase-GR
CaM-activated enzyme CaM kinase II
CaM-dependent kinase
Q84ZT8
CaM-dependent protein kinase
CaM-dependent protein kinase I
CaM-dependent protein kinase II
Cam-II PK
CaM-K I
CaM-K Ialpha
CaM-K II
CaM-K IIalpha
CaM-K IV
CaM-K1delta
Q8IU85
CaM-KI
CaM-KI LiKbeta
CaM-KIalpha
CaM-KII
CaM-kinase I
CaM-kinase II
CaM-kinase III
CaM-kinase IV
CaM-KIV
multifunctional enzyme
CaM-KKbeta3
CaMK II
CaMK IIalpha
Q9UQM7
CaMK IIbeta
CaMK IIdelta
CaMK IIgamma
CaMK IV
camk-1
CaMK-like CREB kinase-III
CaMK1
CAMK2B
Camk2g
Q923T9
CamkG
CaMKI
CaMKIalpha
CaMKIG
CaMKIgamma
CaMKII
CaMKII-alpha
CaMKIIa
isozyme
CaMKIIalpha
CaMKIIbeta
CaMKIId
CaMKIIdelta
CaMKIIdelta2
CaMKIIdeltaA
CaMKIIgamma
CaMKIIgamma G2
CaMKIIgammaB
CaMKIV
CaMKK
Q96RR4
CCaMK
ccamk-1
Medicago truncatula
Q6RET7
CDPK
CLICK-III
CLICK-III/CaMKIgamma
CMK1
CMPK
CPK-1
DMI-3
dmi3-1
kinase, caldesmon (phosphorylating)
kinase, microtubule-associated protein 2 (phosphorylating)
MAP kinase
MAP-2 kinase
MAP-2 protein serine kinase
microtubule associated protein kinase
microtubule-associated protein 2 kinase
peripheral plasma membrane protein CaMGUK
Funaria hygrometrica
TRV25
type II Ca2+/calmodulin-dependent protein kinase
XCaM-KI LiKbeta
XCaM-KIalpha
V5IQT6
Neurospora crassa ATCC 24698
Metarhizium anisopliae
491247, 491248, 491249, 491250, 491251
Electrophorus electricus
664537, 666119, 675969, 693128, 693725, 740328, 740718
Oryctolagus cuniculus
664278, 664472, 664537, 665508, 666114, 666119, 666122, 666132, 666707, 675526, 690363, 691668
Sus scrofa
Q7RVS8, Q7SBJ3, V5IPS5, V5IQT6
Q7RVS8, Q7SBJ3, V5IPS5
Q13555, Q13557
P08413, P11275
Parastagonospora nodorum
Q00LS5
Q96NX5
Q91VB2
Mus musculus C57BL/6
Q9P7I2
Physarum polycephalum
Q8WSQ3
Physarum polycephalum Ng-1
Q59XV1, Q5ANJ0
Candida albicans BWP17
; gene name
Q7RVS8
Q7SBJ3
V5IPS5
Q6PGB8
664537, 665701, 666139, 672940, 674557, 675969, 693128, 693725, 694887, 740328, 740718
664537, 666130, 672384, 672940, 675065, 676849, 693764, 694154, 694372, 694396, 705313, 705318, 722674, 722807, 740886
664472, 664537, 665508, 666114, 666130, 666132, 666707, 671227, 671799, 672850, 672941, 675526, 676041, 676849, 690363, 691668, 721424, 721985, 722760
Q6AX64
Q9DG02
Q5ANJ0
Q59XV1
presumably identical with EC 2.7.1.117
cf. EC 2.7.11.26
the enzyme belongs to the family of CaM-kinases, overview
CLICK-III belongs to the CaMKI family
Ovis aries
presumably identical with casein kinase II
the enzyme belongs to the family of calmodulin-dependent kinases, cf. EC 2.7.11.18
the enzyme is a member of the MAGUK family
ATP + a protein = ADP + a phosphoprotein
catalytic aspartate residue
enzyme appears to be identical with caldesmon; the reaction is an intramolecular autophosphorylation which is site-specific: predominantly serine with some threonine and no tyrosine residues are phosphorylated
Bos taurus
casein kinase II as caldesmon kinase; main phosphorylation site: Ser-73
not identical but with strong binding affinity for caldesmon
p42/p44erk mitogen-activated protein kinase appears to be the major caldesmon kinase, but a yet unidentified kinase, rather than mitogen-activated protein kinase, may be involved in regulation of the caldesmon function in vivo
sequential reaction mechanism in which all substrates bind to enzyme before any product is released. Binding of phospholamban to the enzyme decreases the affinity of the enzyme toward ATP; sequential reaction mechanism in which all substrates bind to enzyme before any product is released. Binding of phospholamban to the enzyme decreases the affinity of the enzyme toward ATP; sequential reaction mechanism in which all substrates bind to enzyme before any product is released. Binding of phospholamban to the enzyme decreases the affinity of the enzyme toward ATP; sequential reaction mechanism in which all substrates bind to enzyme before any product is released. Binding of phospholamban to the enzyme decreases the affinity of the enzyme toward ATP
top print hide show all columns Go to Reaction Type Search
REACTION TYPE
phospho group transfer
ATP:protein phosphotransferase (Ca2+/calmodulin-dependent)
top print hide show all columns Go to CAS Registry Number Search
ATP + 40S-ribosomal protein S6
rat brain
ATP + a protein
ADP + a phosphoprotein
ATP + actin
ADP + phosphoactin
ATP + Akt
ADP + phosphorylated Akt
ATP + alpha-subunit of the cardiac Na+ channel NaV1.5-GST fusion peptide
ADP + phosphorylated alpha-subunit of the cardiac Na+ channel NaV1.5-GST fusion peptide
phosphorylated in vitro by CaMKII predominantly on the I-II linker
ATP + autocamtide-2
ADP + phosphorylated autocamtide-2
ATP + Bcl10
ADP + phosphorylated Bcl10
phosphorylation by CaMKII at Ser138, recombinant FLAG-tagged Bcl10 substrate expressed in HEK-293T cells
ATP + beta-Pak-interacting exchange factor
ADP + phosphorylated beta-Pak-interacting exchange factor
beta-Pak-interacting exchange factor is phosphorylated at Ser156
ATP + biotinylated Thr-Arg-Ser-Ala-Ile-Arg-Arg-Ala-Ser-Thr-Ile-Glu-Met-Pro-Gln-Gln-Ala-Arg-Gln
ADP + biotinylated Thr-Arg-Ser-Ala-Ile-Arg-Arg-Ala-Ser-phospho-Thr-Ile-Glu-Met-Pro-Gln-Gln-Ala-Arg-Gln
biotinylated phospholamban Thr17 peptide substrate
ATP + Blc10
ADP + phosphorylated Blc10
ATP + bovine serum albumin
ADP + phosphorylated bovine serum albumin
low activity
ATP + Ca2+/calmodulin-dependent protein kinase I
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase I
ATP + Ca2+/calmodulin-dependent protein kinase IV
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase IV
ATP + Cabin1
ADP + phosphorylated Cabin1
ATP + caldesmon
ADP + caldesmon phosphate
ATP + cAMP response element binding protein
ADP + phosphorylated cAMP response element binding protein
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
ATP + cAMP-response element-binding protein
ADP + phosphorylated cAMP-response element-binding protein
i.e. CREB, phosphorylation at S133, substrate of CaMKIV and CaMKII
ATP + cAMP-responsive element-binding protein
ADP + phosphorylated cAMP-responsive element-binding protein
ATP + CARMA1
ADP + phosphorylated CARMA1
ATP + casein
ADP + phosphocasein
ADP + phosphorylated casein
ATP + CREB
ADP + phosphorylated CREB
ATP + cyclic AMP response element binding protein
ADP + phosphorylated cyclic AMP response element binding protein
phosphorylated at Ser133
ATP + dystrophin Dp71d
ADP + phosphorylated dystrophin Dp71d
ATP + Emi2
ADP + phosphorylated Emi2
an APC/C repressor, inactivation
ATP + estrogen-receptor from calf uterus
ATP + eukaryotic translation initiation factor 4B
ADP + phosphorylated eukaryotic translation initiation factor 4B
ATP + GABA A receptor
ADP + phosphorylated GABA A receptor
ATP + GABA-modulin
ATP + glutamate receptor subunit GluR1
ADP + phosphorylated glutamate receptor subunit GluR1
ATP + glutamate receptor subunit NR2B
ADP + phosphorylated glutamate receptor subunit NR2B
ATP + glycogen synthase
ADP + phosphorylated glycogen synthase
ATP + glycosylated phosducin-like protein
ADP + glycosylated phosducin-like phosphoprotein
ATP + group I metabotropic glutamate receptor
ADP + phosphorylated group I metabotropic glutamate receptor
CaMKIV contributes to the upregulation of fragile X mental retardation protein induced by stimulating group I metabotropic glutamate receptors
ATP + histone
ADP + phosphohistone
ATP + histone deacetylase 4
ADP + phosphorylated histone deacetylase 4
ATP + histone H1
ADP + phosphorylated histone H1
rat CaMKIV prefers histone H1 over myelin basic protein, while Danio rerio CaMKIV does not
ATP + histone IIA
ADP + phosphorylated histone IIA
ATP + histone IIIS
ADP + phosphorylated histone IIIS
ATP + histone IIS
ADP + phosphorylated histone IIS
ATP + histone VI
ADP + phosphorylated histone VI
ATP + histone VIIS
ADP + phosphorylated histone VIIS
ATP + histone VIS
ADP + phosphorylated histone VIS
ATP + histone VS
ADP + phosphorylated histone VS
ATP + Homer3 protein
ADP + Homer3 phosphoprotein
Homer3 protein is phosphorylated at Ser120, Ser159, and Ser176 by CaMKII
ATP + human cardiac sodium channel NaV1.5
ADP + phosporylated human cardiac sodium channel NaV1.5
ATP + I-kappaB
ADP + phosphorylated I-kappaB
ATP + Kemptide
ADP + LRRAS(P)LG
i.e. LRRASLG, low activity
ATP + Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ADP + phosphorylated Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ATP + KKALRRQETVDAL
ADP + KKALRRQET(P)VDAL
i.e. autocamtide-2
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
ATP + MAP2
ADP + phosphorylated MAP2
ATP + MEF-2A
ADP + phosphorylated MEF-2A
phosphorylation by CaMKIV
ATP + MEF-2C
ADP + phosphorylated MEF-2C
ATP + MEF-2D
ADP + phosphorylated MEF-2D
ATP + microtubule affinity regulating kinase 2
ADP + phosphorylated microtubule affinity regulating kinase 2
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
ATP + microtubule-associated protein tau
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
ATP + myosin
ADP + phosphomyosin
ATP + myosin II light chain
ADP + phosphorylated myosin II light chain
ATP + myosin light chain
ATP + Na+-channel
ADP + phosphorylated Na+-channel
ATP + NADPH oxidase 5
ADP + phosphoraletd NADPH oxidase 5
ATP + neuronal nitric-oxide synthase
ADP + phosphorylated neuronal nitric-oxide synthase
ATP + NFkappaB
ADP + phosphorylated NFkappaB
the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536
ATP + NHE-1
ADP + phosphorylated NHE-1
ATP + NMDA receptor
ADP + phosphorylated NMDA receptor
ATP + Notch1 protein
ADP + phosphorylated Notch1 protein
ATP + PC12 pheochromacytoma cell line protein substrate pp250
ATP + peptide AC2
ADP + phosphorylated peptides AC2
Ca2+-independent autonomous activity after Thr286 autophosphorylation is65% of maximal stimulated activity
ATP + phosphatidylinositol 3-kinase
ADP + phosphorylated phosphatidylinositol 3-kinase
ATP + phospholamban
ADP + phosphorylated phospholamban
ATP + phosvitin
ADP + phosphorylated phosvitin
ATP + PLB
ADP + phosphorylated PLB
a regulatory protein in Ca2+ signaling
ATP + PLN
ADP + phosphorylated PLN
ATP + PLRRTLSVAA
ADP + ?
ATP + PLRRTLSVAA-amide
ADP + phosphorylated PLRRTLSVAA-amide
glycogen synthase-derived peptide GSP
ATP + protamin
ADP + phosphorylated protamin
ATP + protein
ADP + phosphoprotein
ATP + protein CREB
ADP + phosphorylated protein CREB
ATP + protein ERK
ADP + phosphorylated protein ERK
activation by phosphorylation
ATP + protein HDAC
ADP + phosphorylated protein HDAC
ATP + protein kinase B
ADP + phosphorylated protein kinase B
ATP + protein kinase G
ADP + phosphorylated protein kinase G
ATP + protein PLB
ADP + phosphorylated protein PLB
ATP + protein PLN
ADP + phosphorylated Pprotein LN
PLN regulation through phosphorylation by CaMKII at Thr17
ADP + phosphorylated protein PLN
a sarcoplasmic reticulum protein, phosphorylation by CaMKII at Thr17
ATP + protein RyR
ADP + phosphorylated protein RyR
ATP + PSD-95
ADP + phosphorylated PSD-95
ATP + Raf-1 protein
ADP + phosphorylated Raf-1 protein
ATP + ryanodine receptor type 2
ADP + phosphorylated ryanodine receptor type 2
ATP + RyR
ADP + phosphorylated RyR
ATP + S6-kinase
Xenopus sp.
step of a protein kinase cascade initiated by insulin in a yet unidentified manner
ATP + S6-kinase II
ATP + Stargazin
ADP + phosphorylated Stargazin
ATP + STAT3
ADP + phosphorylated STAT3
ATP + stress-induced phosphoprotein 1
ADP + phosphorylated stress-induced phosphoprotein 1
phosphorylated on Ser198
ATP + synapsin
ADP + phosphorylated synapsin
ADP + phosphosynapsin
ATP + synapsin I
ADP + phosphorylated synapsin I
ADP + phosphosynapsin I
ATP + synapsin II
ADP + phosphorylated synapsin II
ATP + synapsin-1
ADP + phopshorylated synapsin-1
ATP + synGAP
ADP + phosphorylated synGAP
ATP + synthide-2
ADP + phorphorylated synthide-2
ATP + syntide-2
ADP + phosphorylated syntide-2
ATP + syntide2
ADP + phosphorylated syntide2
ATP + tau peptide 408-420
ADP + phosphorylated tau peptide 408-420
ATP + tau protein
ADP + phosphorylated tau protein
ATP + tropomyosin
ADP + phosphotropomyosin
ATP + tubulin
ATP + type alpha cytosolic phospholipase A2
ADP + phosphorylated type alpha cytosolic phospholipase A2
CaMK regulates the type alpha cytosolic phospholipase A2 via phosphorylation at Ser515
ATP + vimentin
ADP + phosphorylated vimentin
ATP + voltage-gated calcium channel beta1b subunit
ADP + phosphorylated voltage-gated calcium channel beta1b subunit
ATP + voltage-gated calcium channel beta2a subunit
ADP + phosphorylated voltage-gated calcium channel beta2a subunit
CaMKII phosphorylates at Thr498
ATP + voltage-gated calcium channel beta3 subunit
ADP + phosphorylated voltage-gated calcium channel beta3 subunit
ATP + YLRRRLSDSNF
synapsin site I-derived peptide substrate
the enzyme phosphorylates e.g. the synaptic vesicle-associated protein synapsin 1 and synapsin 2
substrate of CaM-KII, phosphorylation at Thr308
highly selective peptide substrate for calcium/calmodulin-dependent protein kinase II
substrate in activity assay
Bcl10 is essential for antigen receptor-induced NF-kappaB activation, interleukin-2 production, and T-cell proliferation but is not required for TCR-induced tyrosine phosphorylation, calcium flux, or extracellular signal-regulated kinase activation
the enzyme is a member of the CaMK cascade that mediates the response to intracellular Ca2+ elevation. Ca2+/calmodulin-dependent protein kinase kinase phosphorylates and activates Ca2+/calmodulin-dependent protein kinase I and Ca2+/calmodulin-dependent protein kinase IV, which directly activate transcription factors
a transcriptional corepressor of myocyte enhancer factor 2, phosphorylation by CaMKIV creates a docking site for protein 14-3-3, which causes nuclear export, CaMKIV regulates nuclear export of Cabin1 during Ca2+-dependent T-cell activation, regulation overview
a transcriptional corepressor of myocyte enhancer factor 2, phosphorylation at Ser2126 by CaMKIV creates a docking site for protein 14-3-3, which causes nuclear export, no activity with Cabin1 mutant S2126A
less efficient than synapsin
caldesmon plays a role in the regulation of smooth muscle contraction
phosphorylated at 82% the rate of casein
CaMKIV activates CREB by phosphorylation and stimulates CREB-mediated transcription
i.e. CREB
i.e. CREB, phosphorylation by CaMK II at Ser133
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133
i.e. CREB, CaM kinase II, as part of the Ca2+ and CaMK signaling cascade, regulates the phosphorylation of CREB of spinal cord in rats following noxious stimulation, e.g. by capsaicin injection
i.e. CREB, phosphorylation at Ser133
CaMKII is a modulator of CARMA1-mediated NF-kappaB activation, overview
activation by phosphorylation at Ser109, interaction with Bcl10 is facilitated
phosphorylation at about 60% the rate of caldesmon
best substrate
i.e. cAMP-response element binding protein, substrate of CaM-KI, phosphorylation at Ser133
the phosphorylation process involves protein kinase C, EC 2.7.11.13, CAMKII-mediated phosphorylation modulates the Dp71 nuclear localization
a nuclear splicing isoform of Dp71, several potential sites for phosphorylation
low activity, CaMKII, membrane localization of GluR1 restricts its phosphorylation
phosphorylation at Ser831
low activity, CaMKII
H1 (best substrate)
H2a or H2b
V-S
not: 2AS
histone V-S
histone III-S
calf thymus histone II-S, poor substrate
the enzyme may facilitate transcription factor activities by the neutralization of histone deacetylase 4 by phosphorylation, which may contribute to the phenotypic plasticity of gastrointestinal smooth muscle cells
whereas histone deacetylase 5 alone is unresponsive to CaMKII, it becomes responsive to CaMKII in the presence of histone deacetylase 4
the intracellular loop between domains 1 and 2 of cardiac sodium channel NaV1.5 is phosphorylated specifically at the Ser516 and Thr594 sites. The phosphorylation status of Ser516 and Thr594 on cardiac sodium channel NaV1.5, is an important mediator of the enzyme-dependent negative shift in cardiac sodium channel NaV1.5
the intracellular loop between domains 1 and 2 of cardiac sodium channel NaV1.5 is phosphorylated specifically at the Ser516 and Thr594 sites
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
substrate of CaM-KII
phosphorylation of Kir6.2 subunit of cardiac ATP-sensitive potassium channel promotes endocytosis of cardiac ATP-sensitive potassium channels
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
inactivation by CaMKII
CaMKIalpha/microtubule affinity regulating kinase 2 signaling cascade mediates calcium-dependent neurite outgrowth/axonal extension
i.e. MARK2, recombinant myc-tagged MARK2 expressed in HEK-293 cells, mutational determination of phosphorylation sites, overview
Aplysia californica
as good as myelin basic protein
rat brain: broad specificity
ATP preferred to GTP
not MAP-1
phosphorylation sites are serine and threonine
i.e. MAP-2, preferred substrate
Ca2+/calmodulin dependent autophosphorylation
all 4 tau-species, but about 50% of tau1 and tau2 protein remains resistant to phosphorylation
phosphorylation sites: serine
phosphorylation sites: threonine
isolated light chain of smooth-muscle myosin, phosphorylated at 80% the rate of caldesmon
recombinant substrate from Physarum polycephalum, phosphorylation at Ser18, phosphorylation site analysis, no phosphorylation of substrate mutant S18A
smooth-muscle, myosin, rat brain
smooth-muscle, cardiac
smooth-muscle, skeletal muscle
isozyme CaMKIIdelta increases persistent/late inward INa and intracellular Na+ concentration regulazing Na+ channel activity, CaMKII expression is increased in heart failure and may be involved in Na+ channel regulation alterations via calmodulin, overview
the enzyme mediates the phosphorylation and activation of NADPH oxidase 5. The ability of Ca2+/calmodulin-dependent protein kinase to regulate NADPH oxidase 5 activity may be significant in the regulation of production of reactive oxygen species that occurs downstream of calcium-mobilizing agonists such as angiotensin II. Of these phosphorylation sites, mutation of only Ser475 to alanine prevents Ca2+/calmodulin-dependent protein kinase-induced increases in activity of NADPH oxidase 5
phosphorylation on Thr494, Ser498, Ser475, Ser502, and Ser675
phosphorylation at Ser741 by CaM-K Ialpha, wild-type and truncation mutant 1-293 inhibits neuronal nitric-oxide synthase, nNOS, no substrate of CaM-K IIalpha and CaM-K IV
phosphorylation at Ser741 by CaM-K Ialpha, wild-type and truncation mutant 1-293 inhibits neuronal nitric-oxide synthase, nNOS, no substrate of CaM-K IIalpha and CaM-K IV, determination of phosphorylation sites by analytical SDS-PAGE
phosphorylation by CaMKII is regulated by phosphatase PP1 which is associated with the exchanger
a Na+-H+-exchanging protein, phosphorylation by CaMKII at the intracellular cytoplasmic domain
phosphorylation of Notch1 intracellular domain inhibits the proteasomal degradation of Notch1 intracellular domain through Fbw7 ubiquitin-protein ligase complex. Upregulated Notch1 intracellular domain accelerates osteoclast differentiation
phosphorylation by CaMKII activates the sarcoplasmic reticulum Ca2+-ATPase, increasing both the rate of Ca2+ clearance from the myoplasm and the frequency of localized Ca2+ release events from intracellular stores
phosphorylation contributes to mechanical recovery from acidosis by inhibiting SERCA2a inhibition
autophosphorylation at Thr177
autophosphorylation of Ca2+/calmodulin-dependent protein kinase II converts the enzyme to a Ca2+-independent form, autophosphorylation site is Thr286 in the alpha subunit
CaMKII regulates the phosphorylation of CREB in NMDA-induced retinal neurotoxicity
i.e. cyclic AMP-response element binding protein
phosphorylation by nuclear CaMKII results in HDAC translocation from nucleus to cytoplasm
nuclear CaMKII
high activity, CaMKII, smaller synapses show greater variability in PSD-95 phosphorylation
a protein implicated in the scaffolding and trafficking of AMPA receptors
the enzyme phosphorylates Raf-1 at Ser338 and mediates Ras-stimulated Raf-1 activation
i.e. RyR2
phosphorylation sites: serine and threonine
high activity, CaMKII, phosphatases limit phosphorylation of stargazin
brain synapsin best substrate of chicken gizzard caldesmon kinase
brain synapsin best substrate, phosphorylated at 950% the rate of caldesmon
substrate of CaM-KI
regulation and activation of the neuron-specific Ras GTPase-activating protein, synGAP, by phosphorylation through CaMKII in the postsynaptic density fraction of the forebrain, synGAP is part of the signaling complex attached to the cytoplasmic tail of the N-methyl-D-aspartate-type glutamate receptor, overview
activation of the neuron-specific Ras GTPase-activating protein, synGAP, by phosphorylation through CaMKII at Ser1123, Ser1058, Ser750, Ser751, Ser756, Ser764, and Ser/65, reduced activity with synGAP serines phosphorylation site mutants, determination of phosphorylation sites by mass spectrometry, overview
a peptide containing the R-X-X-S/T consensus phosphorylation site 2 of glycogen synthase within the sequence
i.e. PLARTLSVAGLPGKK
i.e. PLARTLSVAGLPGKK, synthetic peptide substrate
a peptide substrate
recombinant substrate expressed in Escherichia coli, phosphorylation at Ser416 by CaM kinase II, no activity with the peptide by CDK5, EC 2.7.11.22, and casein kinase II, EC 2.7.11.26
phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development, CaM kinase II is involved in the accumulation of tau in neuronal soma in Alzheimer's disease brain
recombinant substrate expressed in Escherichia coli, determination of phosphorylation sites, phosphorylation at Ser416 by CaM kinase II, tau is also a substrate for CDK5, EC 2.7.11.22, and casein kinase II, EC 2.7.11.26
phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development
specific phosphorylation by CaMKII at Ser82
specific phosphorylation by CaMKII at Ser82, wild-type vimentin protein and a construct of a vimentin peptide containing Ser82 fused to the NMDA receptor 2B subunit, an interaction partner of CaMKII
generation of Ca2+-independent activity after Thr286 autophosphorylation is a vital step in regulating synaptic plasticity and learning and memory. The autonomy is substrate-dependent, and low autonomy (15-25%) is the general default
the enzyme performs Ca2+/calmodulin-dependent autophosphorylation at a Ser residue
CaMKII induces changes of Na+ channel gating
the C-terminal region of rat CaMKIV, which is absent from Danio rerio CaMKIV, is involved in the regulation of both its substrate specificity and its susceptibility to dephosphorylation by nuclear CaMK phosphatase
involved in neuroplasticity. Mutant caki flies show reduced walking speed in 'Buridan's paradigm'
CaM kinase II plays a role in diverse cellular processes, overview
CaMKII is crucial for cellular and behavioral plasticity, autophosphorylation renders the enzyme independent on Ca2+ and calmodulin, which allows it to act as a molecular memory switch, CaMKII is required for memory formation of the brain in specific neurons, Ca2+-independent CaMKII mutant T287D in the adult Drosophila melanogaster CNS enhances plasticity and the training of pheromonal cues, mechanism, overview
CaM kinase II is strongly phosphorylated by protein kinase A PKA, EC 2.7.11.11, in electrocyte membranes, the activated CaM kinase II 2fold activates the Ca2+ pump and ATPase in the membranes, overview
substrate specificity
protein kinases and protein phosphatases regulate enzyme activities in the cell, overview
the enzyme prefers lysine-rich substrates, no activity with phosvitin and bovine serum albumin, the enzyme performs strictly Ca2+-dependent autophosphorylation which is influenced by substrates, overview
no substrates are bovine cardiac C-protein, bovine brain fodrin, rabbit skeletal muscle glycogen synthase, phosphorylase B, troponon (I + T + C), actin, tropomyosin, smooth muscle actin, filamin, vinculin, alpha-actinin, protamine or phosvitin
caldesmon is not a substrate of smooth-muscle myosin light-chain kinase
isozyme of calmodulin-dependent multifunctional protein kinase II in smooth-muscle
Ca2+ signaling in T-cell activation involves transcriptional activity of MEF-2 and NFAT, which is repressed by Cabin1, activated CaMKIV can overcome the repression by Cabin1, crosstalk between Cabin1 and CaMKIV, dissociation of Cabin1 from MEF-2 by the enzyme requires calmodulin, overview
CaM-KI and calcium/calmodulin-dependent kinase kinase CaM-KK participate in the control of cell cycle progression in MCF-7 human breast cancer cells, CaM-KK controls the G0-G1 restriction check point
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy, CaMKIIdeltaB expression is increased in heart failure, about 2fold in failing cardiomyopathy, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
components of the Ca2+/calmodulin-dependent protein kinase cascade, overview
the enzyme is regulated by Ca2+/calmodulin binding and reversible phosphorylation, overview, the autonomous, Ca2+/calmodulin-independent activity of autophosphorylated Ca2+/calmodulin-dependent protein kinase IV is required for its role in transcription
CaM-K1delta performs autophosphorylation in a Ca2+/calmodulin-dependent manner which has no impact on its kinase activity
CaMKII is a multifunctional enzyme
CaMKII is a major component of the postsynaptic density of excitatory synapses, and plays a key role in the regulation of synaptic function in the mammalian brain, the unique molecular architecture of the postsynaptic density results in highly selective substrate discrimination by CaMKII, overview
CaMKII substrates CARMA1 and Bcl10 functionally interact and control NF-kappaB signaling downstream of the T-cell receptor
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
CaMKII performs autophosphorylation, and may also regulate Na+ channels, overview
CaMKII regulates P/Q-type Ca2+ current in neurons
CaMKIIgamma is activated by autophosphorylation
isozyme CaMKI is activated upon phosphorylation by CaMK kinase on Thr-177 located in activation loop
isozyme CaMKII is activated upon autophosphorylation on Thr-286 located in autoinhibitory domain
isozyme CaMKIV is activated upon phosphorylation by CaMK kinase on Thr-196 located in activation loop
CaMKII binds directly to a site in the C-terminal domain of CaV2.1 channels, autophosphorylation of CaMKII stimulates binding to this site. Autophosphorylated CaMKII can bind to the CaV2.1 channel and synapsin-1 simultaneously. Binding of CaV2.1 to CaMKII induces Ca2+-independent kinase activity, which mediates both autophosphorylation and phosphorylation of synapsin-1 at Ser603. Binding of autophosphorylated CaMKII to GST-tagged CaV2.1(1848–1964) is substantially greater than binding of nonactivated CaMKII. CaM is not required for CaMKII binding to Ca2+channels. Binding of autophosphorylated CaMKII persists after Ca2+/CaM dissociation
substrate specificity and binding structure, the enzyme depends on basic residues for substrate recognition, autoregulation by a pseudosubstrate mechanism, overview
the enzyme performs autophosphorylation
calmodulin-dependent kinase kinase/calmodulin kinase I activity, not CaMKIV or CaMKII, gates extracellular-signal-regulated kinase-dependent long-term potentiation required for learning and memory, Ras-GRF1 and ERK are also involved, NMDA-dependent activation of ERK, CaMKK pathway regulation, overview
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
CaMKII is required for gene transcription induced in the hippocampus by contextual fear conditioning, alphaCaMKII autophosphorylation is required for memory consolidation-specific transcription and formation of long term potentiation and memory, molecular mechanism, overview
CaMKIV regulation, overview, CaMKIV functions as a potent stimulator of Ca2+-dependent gene expression
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
CaMKII performs autophosphorylation
isozyme-selective CaMKII binding sequence for interaction with ligand proteins, overview
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
CaMKI isozymes play distinct roles in hippocampal dendritic growth and neuronal development, overview
CaMKII is critical in regulating myocyte function with regard to excitation-contraction-relaxation cycles and excitation-transcription coupling
CaMKII isozymes have distinct cellular localizations and function, overview, release of acetylcholine from dual transmitting sympathetic neurons requires activation of both the p75 receptor and activated CaMKII, model for neurotrophin-dependent modulation of cholinergic transmission, neurotrophins can influence CaMKII signaling by regulating the production of CaMKII protein and/or by changing the level of CaMKII activation, overview
the enzyme is involved in dendritogenesis in cortical neurons and is required for brain-derived neurotropic factor-stimulated dendritic growth, and regulation of dendritic morphogenesis via the lipid-raft-delineated CL3-STEF-RAc pathway contributing to the development of cortical dendrites, overview
generation of Ca2+-independent autonomous activity by Thr286 autophosphorylation
in terms of substrate specificity, the consensus sequences for phosphorylation by CaMKI, CaMKII, and CaMKIV are quite similar, and hence these kinases sometimes phosphorylate the same substrates, for example cAMP-response element-binding protein. Expression of Camk2g and Camk2d, but not Camk1 or Camk4, in Camk2g-/- eggs leads to degradation of exogenously expressed EMI2
CaMKIIgamma possesses an intrinsic autophosphorylating activity, which renders the enzyme insensitive to changes in intracellular Ca2+ level
the enzyme performs Ca2+/calmodulin-dependent autophosphorylation
CpkA and CpkC are involved in pathogenicity while CpkB is redundant, CpkA is required for pycnidium development
no activity with casein, bovine serum albumin, and light chains of various myosins from Dictyostelium, scallop, Mytilis, and chicken
poor or no substrates are kinesin, myosin I, phosvitin, ATP-citrate lyase
cytoskeletal proteins, e.g. vinculin, filamin, fodrin or neurofilament protein
phosphorylase b
no substrates are protamine
the enzyme is proposed to play a variety of important roles in brain function
CaM kinase II plays a role in diverse cellular processes, the neuronal CaM kinase II is involved in neurotransmitter synthesis and release, modulation of ion cannel activity, cellular transport, cell morphology, regulation of cytoskeleton, and neurite extension, synaptic plasticity, learning and memory, overview, CaM kinase II is involved in memory storage, functional characterization and mechanism, overview, CaMKII is involved in Ca2+-dependent regulation of tyrosine hydroxylase and tryptophan hydroxylase in catecholamin and serotonin biosynthesis, and regulation of monoamine biosynthesis in the brain, CaMKII is involved in PSD in the postsynaptic space, functional analysis including the ion channel activity regulation, e.g. of the NMDA receptor and its NR2B subunit, the glutamate receptor, and the AMPA receptor, and postsynaptic signaling, overview
CaMKIgamma is involved in Ca2+ signal transduction in the cytoplasmic compartment of certain neuronal populations
CaMKII Ca2+/calmodulin-dependently potentiates ATP responses by promoting trafficking of P2X3 receptors, electrical stimulation of dorsal root ganglion neurons or the sciatic nerve enhances the CaMKII-dependent receptor expression in membranes, overview
CaMKII is involved in calcium signaling, synaptic plasticity, learning, and memory, CaMKII activity and expression are altered in the hippocampus of Pb2+-exposed rats, reaction velocity is reduced by 41% and substrate affinity is increased by 22%, the rats exhibit deficits in hippocampal log-term potentiation and spatial learning
CaMKII is reversibly, Ca2+/calmodulin-independently autophosphorylated at Thr286alpha and Thr287beta with inhibitory effect, inactivated and made sedimentable by acute neuronal excitation in rats in vivo, regulation, overview
CASK in inhibited by the plasma membrane Ca2+ pump 4b/CI, PMCA4b, via direct interaction with the C-terminus of the Ca2+ transporter
glutamate receptor stimulation induces Ca2+-dependent CaMKII translocation to synaptic and nonsynaptic sites
isozyme CaMKIIdelta3 is involved in the expression of brain-derive neurotrophic factor, BDNF, in the substantia nigra
the phosphatidylinositol-linked dopamine receptor is involved in regulation of CaMK II enzyme activity in the brain
CaMKII performs autophosphorylation at Thr286
CaMKII is involved in phorbol ester/ionomycin-induced NFkappaB activation, overview
CaMKII kinase modulates PC12 cell neuronal differentiation
CaMKII signaling, overview, CaMKII is essential in the increasing of Ca2+ transient amplitude and production of mechanical contractile recovery from acidosis, two mechanisms, overview
isozyme CaMKIIdelta regulates cell proliferation of vascular smooth muscle cells, overview
N-methyl-D-aspartate-induced neurotoxicity in the rat retina leads to increased levels of phopshorylated CaMKII and susequently of phosphorylated CREB, overview
the enzyme performs autophosphorylation at Thr286 activating the enzyme activity, and at Thr305/Thr306, which inhibits calmodulin binding and enzyme activation
autophosphorylation is not dependent on calmodulin and Ca2+
activated/autophosphorylated CaMKII does not bind to voltage-gated calcium channel subunits beta3 or beta4 subunits
CaMKIIgamma G2 autophosphorylates in the presence of Ca2+/calmodulin and ATP
small C-terminal domain phosphatase-3 dephosphorylates CaMKIIgamma G2, the dephosphorylation is site-specific, excluding the Thr287 associated with Ca2+/calmodulin-independent activation of the kinase, as a result the autonomous activity of CaMKIIgamma G-2 is not affected by the phosphatase activity of small C-terminal domain phosphatase-3
Thr286-autophosphorylation is antagonistic to CaMKII clustering
may be important in cell cycle progression
CaM-KI plays a role in cell structure regulation during early embryonic development
calmodulin/CaMKII and ANG II regulate surface expression, recycling, and functional activity of ion channel NBCe1 via separate mechanisms, CaMKII activates NBCe1 expression, overview
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NATURAL SUBSTRATE
3-phosphoinositide
enzyme is dependent on
Calmodulin
the ATP-binding site is influenced by the autoinhibitory conformation
dependent on
664278, 664472, 664537, 664865, 664935, 665508, 665662, 666110, 666114, 666119, 666130, 666132, 666401, 666459, 666707, 671799, 672850, 672941, 675526, 675548, 676041, 676849, 690363, 690372, 690822, 690926, 691560, 691673, 693768, 694370
664506, 664537, 664750, 664865, 664928, 665484, 665624, 665701, 666119, 666139, 672940, 674557, 675969, 691539, 691612, 691719, 691837, 692226, 692345, 693128, 693725, 694887, 703406, 740003, 740328, 740718
664537, 664865, 665484, 665541, 665662, 666130, 666454, 672384, 672940, 675034, 675065, 676174, 676849, 693760, 693764, 694154, 694372, 694396, 705313, 705318, 705904, 740270, 740886, 741420
binding required for activity
after autophosphorylation, the enzyme is active in the absence of Ca2+/calmodulin and even in the presence of EGTA; requirement
dependent on; dependent on; dependent on
dependent on; dependent on
dependent on, 2 mM CaCl2 plus 0.001 mM calmodulin induce 69.2% activation of CaMKIV activity
substrate activation, but not autophosphorylation is dependent on calmodulin
690363, 690372, 690822, 690926, 691560, 691668, 691673, 694370
a ubiquitous Ca2+-sensing protein called calmodulin (CaM), which contains four EF-hand Ca2+-binding motifs, undergoes conformational change upon Ca2+-binding, and the resulting Ca2+/CaM complex regulates a number of effector proteins including Ca2+/CaM-dependent protein kinases (Ca2+/CaMKs); a ubiquitous Ca2+-sensing protein called calmodulin (CaM), which contains four EF-hand Ca2+-binding motifs, undergoes conformational change upon Ca2+-binding, and the resulting Ca2+/CaM complex regulates a number of effector proteins including Ca2+/CaM-dependent protein kinases (Ca2+/CaMKs); a ubiquitous Ca2+-sensing protein called calmodulin (CaM), which contains four EF-hand Ca2+-binding motifs, undergoes conformational change upon Ca2+-binding, and the resulting Ca2+/CaM complex regulates a number of effector proteins including Ca2+/CaM-dependent protein kinases (Ca2+/CaMKs); a ubiquitous Ca2+-sensing protein called calmodulin (CaM), which contains four EF-hand Ca2+-binding motifs, undergoes conformational change upon Ca2+-binding, and the resulting Ca2+/CaM complex regulates a number of effector proteins including Ca2+/CaM-dependent protein kinases (Ca2+/CaMKs)
calcium-calmodulin dependent signalling via Ca2+ leads to activation of CAMKIV autoinhibition
CaV2.1(1848–1964) contains an IQ-like motif as part of a bipartite regulatory site that is important for CaM-induced facilitation and inactivation of CaV2.1 channels. IQ-like motifs bind CaM. CaM is not required for CaMKII binding to Ca2+channels
each kinase subunit is activated separately by direct binding of Ca2+/CaM, which can also induce intra-holoenzyme inter-subunit Thr286 autophosphorylation
required, calcium-dependent CaM binding overrides the effects of autophosphorylation and activates the protein
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Ca2+
KCl-induced cell depolarization stimulates Dp71d phosphorylation
Mg2+
Mn2+
Pb2+
CaMKII activity and expression are altered in the hippocampus of Pb2+-exposed rats, reaction velocity is reduced by 41% and substrate affinity is increased by 22%, the rats exhibit deficits in hippocampal log-term potentiation and spatial learning, the content of CaMKIIbeta, but not of CaMKIIalpha, in the cytosolic fraction is reduced
little or no effect by Ni2+, Ba2+, Zn2+, Cu2+, and Cd2+
dependent on, binding structure and kinetics
Ca2+/calmodulin-dependent
dependent on, activates
activity becomes partially independent of Ca2+ after autophosphorylation; Ca2+/calmodulin-dependent
the unphosphorylated CaMK1 is dependent on Ca2+ and calmodulin, while the autophosphorylated enzyme is not
dependent on, high affinity to
dependent on, activates, optimal at 0.05 mM
Ca2+/calmodulin-dependent; Ca2+/calmodulin-dependent
Ca2+/calmodulin-dependent; the enzyme responds directly to Ca2+-calmodulin with increased activity
dependent on, Ca2+/calmodulin activate CaMKII prior to autophosphorylation which renders the enzyme independent of Ca2+/calmodulin
absolutely dependent on
dependent on, activates, the Ca2+/calmodulin-binding domain overlaps with the autoinhibition domain
dependent on, activates the nonphosphorylated CaMKIV, the autoinhibitory domain harbors the binding site for Ca2+ and calmodulin
4.42 mM stimulates activity
664506, 664865, 665701, 666119, 672940, 675969, 691612, 691719, 691837, 692345, 693128, 693725, 694887


A couple days ago one of my best friends ( inneedofescape) and I decided to hit up Trona.
80% of Trona is abandoned. The town smells like sulfur and there are constant booming and clanging sounds from the 3 factories. Grass does not grow in Trona...the high school football field is dirt. The locals are drunks and tweakers and will circle a newer model car like vultures circling a dying animal. In summer, temperatures soar to over 120 degrees. It is truly the first layer of Hell.
We thought that one up while driving back from Ridgecrest, which is 20 miles southwest of Trona and the closest source of any amenities (read: Starbucks and Walmart) for the Trona populace. Clever girls we are!
In Trona, one will find that most of the abandoned houses are sort of like the Rapture hit.. people left behind appliances, furniture, cars, RVs..
In this particular house, they had apparently been in the middle of baking a snack when they decided to up and leave.
They left a sink full of dishes, a cupboard full of spices..
They didn't even take their shoes.
They also left behind alot of medication.. of the medications I found were asthma treatments and diuretics.
At this point, the sun was going down, and Trona after dark sounded like a bad horror movie premise.. so we headed out. Very cool, very bizarre place to visit though.. just keep an eye on your car (seriously) and don't go alone.
That's a weird place, the house with the abandoned chips & oven mitt particularly! Why the abandonment, there must be a reason why people abandoned their houses in a hurry or in a non-systematic/organised way? Was there danger (e.g. gases) from the factories or something? Would love to know the story behind it.
They left so suddenly that they left their fries in the oven. That's so creepy, I love this town!
There's so much about this that disturbs me and it takes a lot more to do that then the normal abandoned photos *shudder* I'd pay money to never go here.
For some reason this is completely creeping me out, even though the photos have been taken in broad daylight.
What's the story behind the abandonment? I just did a really quick google search but couldn't see anything.
tronaca.com explains some of it. I really had/have no idea what Trona's story is.. squid_ink found that and it definitely sheds some light.
Great images...glad you made it out okay to post them.
I'm always amazed by the things people leave behind in abandoned houses, but the one with the chips in the oven and all the food left in the cupboards is certainly the weirdest. I'd love to know the story behind it, what caused them to leave in such a hurry and never return.
Thank you :D he's a great exploring buddy too!
I live about an hour from Trona.. in Cal City.
Creepy place, has a feel of a post apocalyptic movie.
That's a great description...these pictures are haunting. Seeing abandoned toys makes me sad. At first I thought this city was somewhere in Australia for some reason but then I saw the California liscense plate. It's creepier to think of people just up and leaving all that stuff behind.
What state is this in? California?
There is an abandoned truck with California plates on it so I'd guess it lived and died there.
It enrages me that man has managed to annihilate what looks like what could have been a pretty nice place to live at one time, even with the intense heat. It's not for everyone but some people like it or at least don't mind it.
You really need to post sad panda bear over at forgotten_toys.
I live in Cal City; I love desert towns and I think Trona would be an awesome place to live if it wasn't so.. dangerous. It's in a really beautiful area.
Go for it! It's only a 15 minute drive from Ridgecrest to Trona.
Thanks for posting! Fascinating stuff.