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So the blue one begins at the five end and goes all the way to the three N, while the pink begins at the three N and goes all the way to the five end. And this is what we mean by the antiparallel directionality, where one of our single stranded DNA runs from the five to three, while the other one runs from the three to five. Now, one other thing that we have to notice is that the sugar as well as the phosphate within our double stranded DNA points outside of that DNA while inside that double stranded DNA double helix structure, we have our nitrogenous basis. So that is shown by the following diagram. So this line basically represents the sugar and the phosphate, while these squares represent our nitrogenous bases. And our nitrogenous bases are basically protected and are found inside our double stranded DNA molecule. | Introduction to DNA.txt |
So that is shown by the following diagram. So this line basically represents the sugar and the phosphate, while these squares represent our nitrogenous bases. And our nitrogenous bases are basically protected and are found inside our double stranded DNA molecule. And that means our bonds can form and those bonds are not disrupted by any type of outside force that is found on the outside of that double stranded DNA molecule. Of course, if we, for example, increase the temperature, eventually a temperature will be reached where these bonds will break, regardless of the fact that our nitrogenous bases are found inside that DNA molecule. So once again, DNA is basically a polymer molecule that contains nucleotides. | Introduction to DNA.txt |
And that means our bonds can form and those bonds are not disrupted by any type of outside force that is found on the outside of that double stranded DNA molecule. Of course, if we, for example, increase the temperature, eventually a temperature will be reached where these bonds will break, regardless of the fact that our nitrogenous bases are found inside that DNA molecule. So once again, DNA is basically a polymer molecule that contains nucleotides. And any given nucleotide consists of three sections. We have the sugar, the nitrogenous base and our phosphate group. And there are four different types of nitrogenous bases. | Introduction to DNA.txt |
And any given nucleotide consists of three sections. We have the sugar, the nitrogenous base and our phosphate group. And there are four different types of nitrogenous bases. The purines are adenine and guanine, while our perimeterines are thymine and cytosine. Now, the way that our two antiparall singlestranded DNA bonds together is via hydrogen bonds between our adjacent nitrogenous bases. So guanine nitrogenous base always forms bonds with cytotine while adenine always forms bonds with thymine. | Introduction to DNA.txt |
So, in this diagram, we actually have two neurons. This is known as the presynaptic neuron, and this is known as the postsynaptic neuron. And so the question is, how can we actually generate an action potential on this membrane of the post synaptic nerve cell? And to begin, let's actually look at this axon terminal of the presynaptic nerve cell. So along the axon HALOCK of this presynaptic nerve cell, an action potential is generated. And that action potential propagates all the way to the axon terminal of this cell. | Generation of Action Potential.txt |
And to begin, let's actually look at this axon terminal of the presynaptic nerve cell. So along the axon HALOCK of this presynaptic nerve cell, an action potential is generated. And that action potential propagates all the way to the axon terminal of this cell. And once at the axon terminal, it basically stimulates the release of hundreds of these vesicles that carry acetylcholine molecules. So these vesicles containing acetylcholine are released into this area known as the synaptic cleft, and it travels along that synaptic cleft, and these acetylcholine ultimately end up binding onto special ligand gated I channels we call acetylcholine receptors, which are these protein membranes shown here. Now, when they bind, they cause the opening of these ligand gated ion channels. | Generation of Action Potential.txt |
And once at the axon terminal, it basically stimulates the release of hundreds of these vesicles that carry acetylcholine molecules. So these vesicles containing acetylcholine are released into this area known as the synaptic cleft, and it travels along that synaptic cleft, and these acetylcholine ultimately end up binding onto special ligand gated I channels we call acetylcholine receptors, which are these protein membranes shown here. Now, when they bind, they cause the opening of these ligand gated ion channels. And the thing about these ligangated ion channels is they're nonspecific. And what that means is they will allow the movement of not only the sodium ions down their electrochemical gradient, but also allow the movement of these potassium down their electrochemical gradient. And so we know that we have many more potassium molecules on the inside than on the outside. | Generation of Action Potential.txt |
And the thing about these ligangated ion channels is they're nonspecific. And what that means is they will allow the movement of not only the sodium ions down their electrochemical gradient, but also allow the movement of these potassium down their electrochemical gradient. And so we know that we have many more potassium molecules on the inside than on the outside. And so these potassium molecules sorry, these potassium mines will move spontaneously in this direction, while at the same time, because we have many more sodium on the outside than the inside, these sodium ions will move spontaneously into the cell. And as they move along their electrochemical gradient, they will cause an increase in the voltage difference across the cell membrane. So remember, for a neuron, the resting membrane potential is around negative 70 millivolts. | Generation of Action Potential.txt |
And so these potassium molecules sorry, these potassium mines will move spontaneously in this direction, while at the same time, because we have many more sodium on the outside than the inside, these sodium ions will move spontaneously into the cell. And as they move along their electrochemical gradient, they will cause an increase in the voltage difference across the cell membrane. So remember, for a neuron, the resting membrane potential is around negative 70 millivolts. And so as a result of this, the voltage will actually begin to increase. Now, if the voltage increases to about negative 40 millivolts, this voltage is known as the threshold voltage. Why? | Generation of Action Potential.txt |
And so as a result of this, the voltage will actually begin to increase. Now, if the voltage increases to about negative 40 millivolts, this voltage is known as the threshold voltage. Why? Well, because this is the voltage that is needed to activate the voltage gated on channels. And this includes not only the sodium, but also the potassium voltage gated on channels. So as the voltage increases from the resting membrane potential of about negative 70 millivolts to about negative 40 millivolts, the voltage gated sodium channels begin to open, and they open very quickly. | Generation of Action Potential.txt |
Well, because this is the voltage that is needed to activate the voltage gated on channels. And this includes not only the sodium, but also the potassium voltage gated on channels. So as the voltage increases from the resting membrane potential of about negative 70 millivolts to about negative 40 millivolts, the voltage gated sodium channels begin to open, and they open very quickly. And this is what initiates the action potential. And the value of negative 70 millivolts is known as the threshold value. So as soon as we reach this threshold value, that will initiate that action potential. | Generation of Action Potential.txt |
And this is what initiates the action potential. And the value of negative 70 millivolts is known as the threshold value. So as soon as we reach this threshold value, that will initiate that action potential. If that value is not reached when this movement takes place, the no action potential is actually generated. So we have to reach that value. So let's assume that value is in fact, reached. | Generation of Action Potential.txt |
If that value is not reached when this movement takes place, the no action potential is actually generated. So we have to reach that value. So let's assume that value is in fact, reached. So once we reach this value, we have a very rapid opening of these sodium voltage gated on channels. So let's take a look at the following diagram. So, when the membrane is at a resting memory potential of negative 70 millivolts, this structure is basically in its closed form. | Generation of Action Potential.txt |
So once we reach this value, we have a very rapid opening of these sodium voltage gated on channels. So let's take a look at the following diagram. So, when the membrane is at a resting memory potential of negative 70 millivolts, this structure is basically in its closed form. And this is the voltage gated sodium ion channel. Now, what happens when we go from this voltage difference to this voltage difference? These paddle domains essentially orient themselves upward. | Generation of Action Potential.txt |
And this is the voltage gated sodium ion channel. Now, what happens when we go from this voltage difference to this voltage difference? These paddle domains essentially orient themselves upward. And as they move from this orientation to this orientation, that opens, that widens that pore on this side of the membrane. And as soon as that pore widens, that creates the open state. And the sodium ions can basically move down their electrochemical gradient from a high outside concentration to a low inside concentration. | Generation of Action Potential.txt |
And as they move from this orientation to this orientation, that opens, that widens that pore on this side of the membrane. And as soon as that pore widens, that creates the open state. And the sodium ions can basically move down their electrochemical gradient from a high outside concentration to a low inside concentration. So basically, this area is known as the depolarization period. And what that means is, because of the rapid opening of many of these voltage gated sodium ion channels, we have a rapid influx of these sodium ions into the cell. And so many of these positively charged sodium ions move into the cell. | Generation of Action Potential.txt |
So basically, this area is known as the depolarization period. And what that means is, because of the rapid opening of many of these voltage gated sodium ion channels, we have a rapid influx of these sodium ions into the cell. And so many of these positively charged sodium ions move into the cell. And that makes the inside of the cell positive with respect to the outside. And that's exactly why we increase the value to about positive 30 millivolts. Now, notice it increases, but we don't actually get to the positive 60 millivolt value, which is what the sodium voltage is at equilibrium. | Generation of Action Potential.txt |
And that makes the inside of the cell positive with respect to the outside. And that's exactly why we increase the value to about positive 30 millivolts. Now, notice it increases, but we don't actually get to the positive 60 millivolt value, which is what the sodium voltage is at equilibrium. And that's because as we begin to approach this value, some of these actually become inactivated. So remember, about a millisecond after we actually open these channels, they begin to close as a result of the occlusion, as a result of the blocking action of this chain. So, based on the ball and chain model, we know that this ball will basically move into that pore and that will block and inactivate the movement of these ions. | Generation of Action Potential.txt |
And that's because as we begin to approach this value, some of these actually become inactivated. So remember, about a millisecond after we actually open these channels, they begin to close as a result of the occlusion, as a result of the blocking action of this chain. So, based on the ball and chain model, we know that this ball will basically move into that pore and that will block and inactivate the movement of these ions. And so that's exactly what happens in this region at the peak of this graph. Now, at the same exact time. Oh, and by the way, if we go back to this section here. | Generation of Action Potential.txt |
And so that's exactly what happens in this region at the peak of this graph. Now, at the same exact time. Oh, and by the way, if we go back to this section here. So here I said that we have the opening of these voltage gated sodium channels, but the voltage gated sodium channels are not the only ones to open. We also have the opening of the potassium voltage gated on channels. But these potassium voltage gate on channels are very, very slow to open. | Generation of Action Potential.txt |
So here I said that we have the opening of these voltage gated sodium channels, but the voltage gated sodium channels are not the only ones to open. We also have the opening of the potassium voltage gated on channels. But these potassium voltage gate on channels are very, very slow to open. On the contrary, the sodium voltage gated on channels open up very, very quickly. And so that's exactly why we have this deep polarization period, a rapid increase to a positive value of that potential. So the opening of the voltage gated sodium channels leads to a rapid rise in the membrane potential. | Generation of Action Potential.txt |
On the contrary, the sodium voltage gated on channels open up very, very quickly. And so that's exactly why we have this deep polarization period, a rapid increase to a positive value of that potential. So the opening of the voltage gated sodium channels leads to a rapid rise in the membrane potential. Now, although the voltage gated potassium channels are slow to open, they too begin to open. But they open very slowly. But after about one millisecond of the opening of these sodium voltage gate on channels, they begin to close as a result of the inactivation of this ball. | Generation of Action Potential.txt |
Now, although the voltage gated potassium channels are slow to open, they too begin to open. But they open very slowly. But after about one millisecond of the opening of these sodium voltage gate on channels, they begin to close as a result of the inactivation of this ball. So this ball domain enters this section and it blocks that pore as shown in this particular diagram. And so now the sodium ion channels, the sodium ions can no longer move into the cell at the same moment in time. So in this region, we have the quickening of the opening process of these potassium voltage gated on channels, and so they begin to open up. | Generation of Action Potential.txt |
So this ball domain enters this section and it blocks that pore as shown in this particular diagram. And so now the sodium ion channels, the sodium ions can no longer move into the cell at the same moment in time. So in this region, we have the quickening of the opening process of these potassium voltage gated on channels, and so they begin to open up. So essentially the same exact thing happens as in this particular case. These paddle domains basically begin to orient themselves as a result of that depolarization of the membrane. And so, when this orients upward, that opens and winds the port at the bottom. | Generation of Action Potential.txt |
So essentially the same exact thing happens as in this particular case. These paddle domains basically begin to orient themselves as a result of that depolarization of the membrane. And so, when this orients upward, that opens and winds the port at the bottom. And that allows the movement of these potassium odds down their electrochemical gradient. And unlike in this case, the electrochemical gradient basically tells us that these potassium mons will move from the inside to the outside of the south. And this takes place here. | Generation of Action Potential.txt |
And that allows the movement of these potassium odds down their electrochemical gradient. And unlike in this case, the electrochemical gradient basically tells us that these potassium mons will move from the inside to the outside of the south. And this takes place here. So basically, what we see happening is the sodium ions can no longer flow into that cell, while at the same time, these potassium ions begin to flow out of the cell. And what that means is the positive charge inside the cell will begin to decrease. And so that means we'll see a drop in that voltage difference between the membrane. | Generation of Action Potential.txt |
So basically, what we see happening is the sodium ions can no longer flow into that cell, while at the same time, these potassium ions begin to flow out of the cell. And what that means is the positive charge inside the cell will begin to decrease. And so that means we'll see a drop in that voltage difference between the membrane. And so, because of that, this is known as the repolarization period. So it tries to repolarize and return that voltage to its resting membrane potential of about negative 70 millivolts. But let's see what happens. | Generation of Action Potential.txt |
And so, because of that, this is known as the repolarization period. So it tries to repolarize and return that voltage to its resting membrane potential of about negative 70 millivolts. But let's see what happens. Notice that it actually drops below the negative 70 millivolts value. And that's because many of these voltage gated potassium ions actually open. And so we have this outflux of these potassium ions out of the cell, and that causes a hyperpolarization period. | Generation of Action Potential.txt |
Notice that it actually drops below the negative 70 millivolts value. And that's because many of these voltage gated potassium ions actually open. And so we have this outflux of these potassium ions out of the cell, and that causes a hyperpolarization period. So hyperpolarization basically means it drops the value below that resting memory potential to a value of about negative 80 millivolts. So the inactivation of the sodium channels and at the same time, the opening of those potassium voltage gated on channels causes the outflux of positive charge out of that cell. And so this rapid drop causes hyperpolarization such that the membrane potential drops below the resting potential of negative 70 millivolts. | Generation of Action Potential.txt |
So hyperpolarization basically means it drops the value below that resting memory potential to a value of about negative 80 millivolts. So the inactivation of the sodium channels and at the same time, the opening of those potassium voltage gated on channels causes the outflux of positive charge out of that cell. And so this rapid drop causes hyperpolarization such that the membrane potential drops below the resting potential of negative 70 millivolts. Now, after about two milliseconds from where everything essentially begun, what begins to happen is as a result of this drop in voltage, these voltage gated potassium ions will begin to close and some of them will also become inactivated in the same method that we discussed here. So the ball will basically enter that port section that will close that channel and will prevent the movement of these potassium potassium ions. And so what happens is, as both of these are closed and inactivated, we'll see that eventually that voltage difference will approach that resting membrane potential. | Generation of Action Potential.txt |
Now, after about two milliseconds from where everything essentially begun, what begins to happen is as a result of this drop in voltage, these voltage gated potassium ions will begin to close and some of them will also become inactivated in the same method that we discussed here. So the ball will basically enter that port section that will close that channel and will prevent the movement of these potassium potassium ions. And so what happens is, as both of these are closed and inactivated, we'll see that eventually that voltage difference will approach that resting membrane potential. In fact, the sodium potassium Atph pump actually is also used to help return this voltage to its original resting membrane potential. And that happens around this section. So, once again, let's summarize how these two types of ion channels, the voltage gated ion channels and the ligand gated ion channels actually work together. | Generation of Action Potential.txt |
In fact, the sodium potassium Atph pump actually is also used to help return this voltage to its original resting membrane potential. And that happens around this section. So, once again, let's summarize how these two types of ion channels, the voltage gated ion channels and the ligand gated ion channels actually work together. And let's take a look at this diagram. So, in this section, we basically have the action of that acetylcholine receptor. So as it is opened up as a result of the binding of that ligand, the acetylcholine, it causes an increase in that voltage value. | Generation of Action Potential.txt |
And let's take a look at this diagram. So, in this section, we basically have the action of that acetylcholine receptor. So as it is opened up as a result of the binding of that ligand, the acetylcholine, it causes an increase in that voltage value. And eventually, if that voltage reaches the threshold voltage, it causes the rapid opening of the voltage gated sodium ion channels. At the same time, it causes a slow opening of those potassium voltage gated ion channels. And so, because we have the rapid opening of these voltage gated sodium ion channels, these sodium ions move into the cell and that makes the inside positive with respect to the outside. | Generation of Action Potential.txt |
And eventually, if that voltage reaches the threshold voltage, it causes the rapid opening of the voltage gated sodium ion channels. At the same time, it causes a slow opening of those potassium voltage gated ion channels. And so, because we have the rapid opening of these voltage gated sodium ion channels, these sodium ions move into the cell and that makes the inside positive with respect to the outside. And that's why it shoots up. And this is known as the depolarization period, because we change the charge values on that cell membrane. So before, during the resting memory potential, the inside was negative, the outside was positive, and now it essentially reverses. | Generation of Action Potential.txt |
And that's why it shoots up. And this is known as the depolarization period, because we change the charge values on that cell membrane. So before, during the resting memory potential, the inside was negative, the outside was positive, and now it essentially reverses. So the inside becomes positive, the outside becomes negative. And that's where we're in this period here. So it reaches a peak of about positive 30 millivolts and it never actually reaches this value here. | Generation of Action Potential.txt |
So the inside becomes positive, the outside becomes negative. And that's where we're in this period here. So it reaches a peak of about positive 30 millivolts and it never actually reaches this value here. And that's because now these become inactivated. So as a result of this ball, it basically goes into that pore and then inactivates that protein. And it basically prevents the movement of those ions across the cell membrane. | Generation of Action Potential.txt |
And that's because now these become inactivated. So as a result of this ball, it basically goes into that pore and then inactivates that protein. And it basically prevents the movement of those ions across the cell membrane. And that happens here. At the same exact time, those voltage gated potassium ions that were slow to open, now open up much, much quicker. And so, because we have the closure of these and the opening of the potassium voltage gate on challenge, now the positive charge begins to move out of the cell. | Generation of Action Potential.txt |
And that happens here. At the same exact time, those voltage gated potassium ions that were slow to open, now open up much, much quicker. And so, because we have the closure of these and the opening of the potassium voltage gate on challenge, now the positive charge begins to move out of the cell. And this is known as repolarization, because as the charge moves out, the inside of the membrane will once again become negatively charged. And so, because we have the inactivation of these potassium of these sodium voltage gate channels and the activation of these potassium voltage gate on channels, it actually goes below that negative 70 millivolt value. And this is known as the hyperpolarization period. | Generation of Action Potential.txt |
And this is known as repolarization, because as the charge moves out, the inside of the membrane will once again become negatively charged. And so, because we have the inactivation of these potassium of these sodium voltage gate channels and the activation of these potassium voltage gate on channels, it actually goes below that negative 70 millivolt value. And this is known as the hyperpolarization period. And eventually there will be a closure and in some cases, an inactivation of these potassium voltage gate on channels. And so that will basically help return that voltage difference back to normal. Of course, with the help of that sodium potassium Atpace pump, eventually that resting membrane potential is returned back to normal to value of negative 70 millivolts. | Generation of Action Potential.txt |
And so this is what I'd like to focus on in this lecture. And I'd like to begin by focusing on a specific digestive enzyme found inside our body known as Chimetrypsin. Now, actually, we already spoke about Chimotrypsin in detail when we discuss proteases. And we said that Chimotrypsin is actually an example of a serene protease that breaks peptide bonds on the carboxyl side of specific amino acids, those amino acids that contain bulky hydrophobic aromatic side chains. Now, Chimetrypsin is initially synthesized in a Zymogen form in the inactive form. And the Zymogen form of China trypsin is known as Chimotrypcinogen. | Proteolytic Activation of Digestive Enzymes .txt |
And we said that Chimotrypsin is actually an example of a serene protease that breaks peptide bonds on the carboxyl side of specific amino acids, those amino acids that contain bulky hydrophobic aromatic side chains. Now, Chimetrypsin is initially synthesized in a Zymogen form in the inactive form. And the Zymogen form of China trypsin is known as Chimotrypcinogen. And Chimitripcinogen is a single polypeptide chain that consists of 245 individual amino acids. Now, the Chimitripcinogen is not fully functional. In fact, it's not functional at all. | Proteolytic Activation of Digestive Enzymes .txt |
And Chimitripcinogen is a single polypeptide chain that consists of 245 individual amino acids. Now, the Chimitripcinogen is not fully functional. In fact, it's not functional at all. And that's because the active side and the oxyanion whole of this particular Zymogen is not yet formed. It's not in the proper confirmation to be able to actually fit this substrate molecule. So what has to happen is this Chimotrypcinogen has to actually be activated proteolytically. | Proteolytic Activation of Digestive Enzymes .txt |
And that's because the active side and the oxyanion whole of this particular Zymogen is not yet formed. It's not in the proper confirmation to be able to actually fit this substrate molecule. So what has to happen is this Chimotrypcinogen has to actually be activated proteolytically. And we'll see how that happens in just a moment. First, let's actually discuss where the Chimotrypcinogen is formed. So if we study the pancreas of our body, in the pancreas, we're going to find these special cells, exercise cells known as acinor cells. | Proteolytic Activation of Digestive Enzymes .txt |
And we'll see how that happens in just a moment. First, let's actually discuss where the Chimotrypcinogen is formed. So if we study the pancreas of our body, in the pancreas, we're going to find these special cells, exercise cells known as acinor cells. And it's the asinr cells of the pancreas which are responsible for forming this Chimetrypcinogen, as well as other digestive zymogens. And all these Xiaomogens are essentially stored in membrane bound organelles, in membrane bound granules shown in green. And so all these granules that contain the zymogens basically accumulate on the apex side of these asinr cells. | Proteolytic Activation of Digestive Enzymes .txt |
And it's the asinr cells of the pancreas which are responsible for forming this Chimetrypcinogen, as well as other digestive zymogens. And all these Xiaomogens are essentially stored in membrane bound organelles, in membrane bound granules shown in green. And so all these granules that contain the zymogens basically accumulate on the apex side of these asinr cells. And when the cell is stimulated by some type of hormone or some type of action potential, these granules basically exit the cell via exocytosis and they release all these zymogens into the duct. And then the duct basically empties out into a larger duct which eventually empties out into the pancreatic duct. And it's the pancreatic duct that connects directly to the initial portion of the small intestine we call the duodenum. | Proteolytic Activation of Digestive Enzymes .txt |
And when the cell is stimulated by some type of hormone or some type of action potential, these granules basically exit the cell via exocytosis and they release all these zymogens into the duct. And then the duct basically empties out into a larger duct which eventually empties out into the pancreatic duct. And it's the pancreatic duct that connects directly to the initial portion of the small intestine we call the duodenum. And once these zymogens are inside the intestine, they only begin to cleave those proteins when the Xiaomogens are activated into their fully functional form. So the question is, how exactly is Chimotryptynogen actually activated proteolytically? Well, as it turns out, interestingly enough, it's actually another active digestive enzyme known as trypsin, another protease that is responsible for activating Chimotrypcinogen into its active form, Chimotrypsin. | Proteolytic Activation of Digestive Enzymes .txt |
And once these zymogens are inside the intestine, they only begin to cleave those proteins when the Xiaomogens are activated into their fully functional form. So the question is, how exactly is Chimotryptynogen actually activated proteolytically? Well, as it turns out, interestingly enough, it's actually another active digestive enzyme known as trypsin, another protease that is responsible for activating Chimotrypcinogen into its active form, Chimotrypsin. So let's take a look at how that actually takes place by looking at the following diagram. So, in part A, we basically have that inactive Zymogen, the Chimotrypcinogen. And notice it consists of 145 individual amino acids. | Proteolytic Activation of Digestive Enzymes .txt |
So let's take a look at how that actually takes place by looking at the following diagram. So, in part A, we basically have that inactive Zymogen, the Chimotrypcinogen. And notice it consists of 145 individual amino acids. So this is not functional because its active side does not have the correct orientation. And the oxyanion hole that is used to basically stabilize the tetrahedral intermediate is not formed. And so what must happen is to actually activate the enzyme activity of this molecule, trypsin and active form another digestive enzyme basically must cleave at a single peptide bond this inactive chymatrypcinogen. | Proteolytic Activation of Digestive Enzymes .txt |
So this is not functional because its active side does not have the correct orientation. And the oxyanion hole that is used to basically stabilize the tetrahedral intermediate is not formed. And so what must happen is to actually activate the enzyme activity of this molecule, trypsin and active form another digestive enzyme basically must cleave at a single peptide bond this inactive chymatrypcinogen. And so what it does is it cleaves the peptide bond between the 15th and the 16th amino acid. Now, the 15th amino acid is arginine and the 16th amino acid is isolucine. So the bond holding these two amino acids is cleaved by Trypsin and this activates this Zymogen to form something we call pychiamitrypsin. | Proteolytic Activation of Digestive Enzymes .txt |
And so what it does is it cleaves the peptide bond between the 15th and the 16th amino acid. Now, the 15th amino acid is arginine and the 16th amino acid is isolucine. So the bond holding these two amino acids is cleaved by Trypsin and this activates this Zymogen to form something we call pychiamitrypsin. Now, Pi chymatrypsin is not yet a fully functional enzyme. What Pi Chimetrypsin does is it goes on to other Pi Chimetrypsin molecules and it cleaves those molecules at several sites. And what it does is it ultimately removes two dipeptides from this molecule. | Proteolytic Activation of Digestive Enzymes .txt |
Now, Pi chymatrypsin is not yet a fully functional enzyme. What Pi Chimetrypsin does is it goes on to other Pi Chimetrypsin molecules and it cleaves those molecules at several sites. And what it does is it ultimately removes two dipeptides from this molecule. So it removes a dipeptide from this region to basically remove two amino acids. That's why we go from 15 to 13 and we also cleave in this section and we remove a dipeptide. And so that's why we have two amino acids missing in this section. | Proteolytic Activation of Digestive Enzymes .txt |
So it removes a dipeptide from this region to basically remove two amino acids. That's why we go from 15 to 13 and we also cleave in this section and we remove a dipeptide. And so that's why we have two amino acids missing in this section. And so once we form these three individual chains these three individual chains are held together by disulfide bonds. And now the active side takes the proper confirmation and the oxyanine hole that is used to stabilize that tetrahedral intermediate takes on that perfect form so that once the active side is formed it can actually fit that substrate intermediate. And once the reaction takes place the tetrahedral intermediate can be stabilized by that fully formed oxyanion hole. | Proteolytic Activation of Digestive Enzymes .txt |
And so once we form these three individual chains these three individual chains are held together by disulfide bonds. And now the active side takes the proper confirmation and the oxyanine hole that is used to stabilize that tetrahedral intermediate takes on that perfect form so that once the active side is formed it can actually fit that substrate intermediate. And once the reaction takes place the tetrahedral intermediate can be stabilized by that fully formed oxyanion hole. So once again, we see that Trypsin cleaves the peptide between the peptide bond between the arginine 15 and the isolucine 16 producing this active pie Chimetrypsin. Now, this active Pychiamatripsin goes on, reacts with another pikmatripsin and that removes two dipeptides to produce a total of three individual chains. And these three chains, which are held together by disulfide bonds basically constitute that fully functional, fully active Chimotrypsin molecule we call Alpha Chimetrypsin. | Proteolytic Activation of Digestive Enzymes .txt |
So once again, we see that Trypsin cleaves the peptide between the peptide bond between the arginine 15 and the isolucine 16 producing this active pie Chimetrypsin. Now, this active Pychiamatripsin goes on, reacts with another pikmatripsin and that removes two dipeptides to produce a total of three individual chains. And these three chains, which are held together by disulfide bonds basically constitute that fully functional, fully active Chimotrypsin molecule we call Alpha Chimetrypsin. Now, what's so different between the active Alpha Chimetrypsin and the inactive Chimetrypsinogen? Well, as it turns out, the active side and the oxyanine hole are not formed correctly in this Zymogen form. And what that proteolytic cleavage does is it allows for a localized conformational change to basically take place within this region. | Proteolytic Activation of Digestive Enzymes .txt |
Now, what's so different between the active Alpha Chimetrypsin and the inactive Chimetrypsinogen? Well, as it turns out, the active side and the oxyanine hole are not formed correctly in this Zymogen form. And what that proteolytic cleavage does is it allows for a localized conformational change to basically take place within this region. And as a result of that localized conformational change that basically creates the proper confirmation of the active side and also creates that oxynine hole that is needed to stabilize the tetrahedral intermediate that is formed in that proteolytic reaction that climate Trypsin actually carries out. So we see that proteolytic activation of Chimotrypsinogen causes a local conformational change that allows the active side and the oxygenine hole to actually form. So we conclude that by proteolytically cleaving this inactive Chimotrypcinogen so the entire structure of this Chimetrypsin doesn't actually change too much. | Proteolytic Activation of Digestive Enzymes .txt |
And as a result of that localized conformational change that basically creates the proper confirmation of the active side and also creates that oxynine hole that is needed to stabilize the tetrahedral intermediate that is formed in that proteolytic reaction that climate Trypsin actually carries out. So we see that proteolytic activation of Chimotrypsinogen causes a local conformational change that allows the active side and the oxygenine hole to actually form. So we conclude that by proteolytically cleaving this inactive Chimotrypcinogen so the entire structure of this Chimetrypsin doesn't actually change too much. But because of a small localized change in this section of that enzyme that creates a perfect active that can fit the substrate molecule and also creates the oxygen hole that will be used by the Chimetrypsin to basically stabilize and decrease that transition state that is formed in that proteolytic reaction that is carried out that is carried out by the digestive enzyme climate trypsin. Now, this is only one of the many different types of digestive enzymes that exist inside our body. And the reason we have these different digestive enzymes is because each digestive enzyme has a slightly different specificity. | Proteolytic Activation of Digestive Enzymes .txt |
But because of a small localized change in this section of that enzyme that creates a perfect active that can fit the substrate molecule and also creates the oxygen hole that will be used by the Chimetrypsin to basically stabilize and decrease that transition state that is formed in that proteolytic reaction that is carried out that is carried out by the digestive enzyme climate trypsin. Now, this is only one of the many different types of digestive enzymes that exist inside our body. And the reason we have these different digestive enzymes is because each digestive enzyme has a slightly different specificity. And we need all these different enzymes to be able to cleave all the different peptide bonds that are found within the proteins that we actually ingest. And the interesting thing about the trypsin molecule that we discussed earlier, trypsin doesn't only activate the chinatriptcinogen, it also activates many other zymogens. And so in a way, we can imagine that trypsin is actually the master activator which is responsible for actually activating the majority of the xiaogens found inside our body. | Proteolytic Activation of Digestive Enzymes .txt |
And we need all these different enzymes to be able to cleave all the different peptide bonds that are found within the proteins that we actually ingest. And the interesting thing about the trypsin molecule that we discussed earlier, trypsin doesn't only activate the chinatriptcinogen, it also activates many other zymogens. And so in a way, we can imagine that trypsin is actually the master activator which is responsible for actually activating the majority of the xiaogens found inside our body. Now, the question is what activates the trypsin itself? Well, the cells of our body basically produce a special type of enzyme known as anterappeptidase. So it's the anteripeptidase that is produced by our body that actually activates trypsin from tryptinogen. | Proteolytic Activation of Digestive Enzymes .txt |
Now, the question is what activates the trypsin itself? Well, the cells of our body basically produce a special type of enzyme known as anterappeptidase. So it's the anteripeptidase that is produced by our body that actually activates trypsin from tryptinogen. Remember, tryptogen is the xiaomogen, the inactive form of trypsin. And when anteripeptidase basically proteolytically cleaves a bond in trypsin, the entire structure of the trips, ingen or not trypsin tryptogen, the entire structure of the trypsinogen changes and that creates the proper confirmation of the active side that now allows that trips and to basically carry out its activity. And what trypsin does is it activates not only for other different xiaomages, but it also activates itself. | Proteolytic Activation of Digestive Enzymes .txt |
Remember, tryptogen is the xiaomogen, the inactive form of trypsin. And when anteripeptidase basically proteolytically cleaves a bond in trypsin, the entire structure of the trips, ingen or not trypsin tryptogen, the entire structure of the trypsinogen changes and that creates the proper confirmation of the active side that now allows that trips and to basically carry out its activity. And what trypsin does is it activates not only for other different xiaomages, but it also activates itself. Trypsin, once activated, basically goes on to nearby tryptogen molecules and activates them to produce trypsin. So this is an amplification effect. And trypsin can also go on to activate proelastates into elastics climate trypsynogen into chimetrypsin, which we spoke about just a moment ago. | Proteolytic Activation of Digestive Enzymes .txt |
Trypsin, once activated, basically goes on to nearby tryptogen molecules and activates them to produce trypsin. So this is an amplification effect. And trypsin can also go on to activate proelastates into elastics climate trypsynogen into chimetrypsin, which we spoke about just a moment ago. Prolipase, which activates lipase and lipase is used to basically break down the lipids that we ingest into our body and finally procarboxy peptidase into carboxy peptidase. So we see that tryptin is the master activator that proteolytically activates the majority of the digestive enzymes, including itself. And Trypton itself is activated by interate peptidase. | Proteolytic Activation of Digestive Enzymes .txt |
Firstly, it protects our body from different pathogenic infections and filters our blood from pathogenic agents that can essentially cause harm to our body and the cells of our body. And secondly, the Lymphatic system also maintains fluid homeostates. Specifically, what it does is it prevents the buildup of fluid from taking place inside the tissues of our body. Now, to see exactly what we mean by that, let's take a look at the following diagram. This diagram describes the cells of some particular tissue and the cells are shown in brown. It also describes the capillary system that is found within our tissue. | Lymphatic System .txt |
Now, to see exactly what we mean by that, let's take a look at the following diagram. This diagram describes the cells of some particular tissue and the cells are shown in brown. It also describes the capillary system that is found within our tissue. And wherever we have a capillary system, we also have a Lymph system. And the vessel of the Lymph system is shown in green. So basically, we have the arterial, the blood vessel shown in red, that brings the oxygenated and the nutrient filled blood to the capillary of our blood vessel system. | Lymphatic System .txt |
And wherever we have a capillary system, we also have a Lymph system. And the vessel of the Lymph system is shown in green. So basically, we have the arterial, the blood vessel shown in red, that brings the oxygenated and the nutrient filled blood to the capillary of our blood vessel system. And within the capillary, we have exchange between nutrients and wastes taking place. And then the Venuel is the blood vessel that carries the deoxygenated blood that contains the waste products back to the heart. So let's recall how the exchange of nutrients and waste products takes place within our capillary. | Lymphatic System .txt |
And within the capillary, we have exchange between nutrients and wastes taking place. And then the Venuel is the blood vessel that carries the deoxygenated blood that contains the waste products back to the heart. So let's recall how the exchange of nutrients and waste products takes place within our capillary. So, if we examine the arterial side of the capillary, on the arterial side, we have a higher hydrostatic pressure than osmotic pressure. And that's exactly why that hydrostatic pressure is able to force the blood plasma that contains the nutrients and our oxygen from the capillary and into the surrounding tissue space. And the surrounding tissue space is known as the interstitial tissue. | Lymphatic System .txt |
So, if we examine the arterial side of the capillary, on the arterial side, we have a higher hydrostatic pressure than osmotic pressure. And that's exactly why that hydrostatic pressure is able to force the blood plasma that contains the nutrients and our oxygen from the capillary and into the surrounding tissue space. And the surrounding tissue space is known as the interstitial tissue. So what happens is when the blood plasma leaves the capillaries and enters this cell tissue area, that brings the nutrients, such as glucose and fats and amino acids and oxygen to the cells of that surrounding tissue. And at the same time as that fluid travels along the tissue space, along the interstitial tissue, it picks up those waste products that are secreted by the cell, such as carbon dioxide and ammonia. And once the fluid is on the Venuel side, on this side of the capillary, because the zmotic pressure is now greater than the hydrostatic pressure, the blood rushes back into the capillary of our body. | Lymphatic System .txt |
So what happens is when the blood plasma leaves the capillaries and enters this cell tissue area, that brings the nutrients, such as glucose and fats and amino acids and oxygen to the cells of that surrounding tissue. And at the same time as that fluid travels along the tissue space, along the interstitial tissue, it picks up those waste products that are secreted by the cell, such as carbon dioxide and ammonia. And once the fluid is on the Venuel side, on this side of the capillary, because the zmotic pressure is now greater than the hydrostatic pressure, the blood rushes back into the capillary of our body. And now the deoxygenated blood that contains the waste products travels along the Venuel, then to the veins and finally into the heart of our body. Now, it turns out that osmotic pressure on the Venuel side is not that much higher than the hydrostatic pressure. And what that means is not all of that blood plasma that left the capillary actually returns back into that capillary on the Venuel side. | Lymphatic System .txt |
And now the deoxygenated blood that contains the waste products travels along the Venuel, then to the veins and finally into the heart of our body. Now, it turns out that osmotic pressure on the Venuel side is not that much higher than the hydrostatic pressure. And what that means is not all of that blood plasma that left the capillary actually returns back into that capillary on the Venuel side. In fact, about 10% of that fluid that left the capillary and entered our tissue will remain in that interstitial space, in the space surrounding our capillary. The question is, what happens to this 10% fluid if this 10% fluid is not removed in any way, there will be a build up of pressure as a result of the build up of fluid inside that tissue. And that will lead to swelling, the process of edema. | Lymphatic System .txt |
In fact, about 10% of that fluid that left the capillary and entered our tissue will remain in that interstitial space, in the space surrounding our capillary. The question is, what happens to this 10% fluid if this 10% fluid is not removed in any way, there will be a build up of pressure as a result of the build up of fluid inside that tissue. And that will lead to swelling, the process of edema. And that can lead to very serious medical conditions and medical complications. So to prevent this from happening, what our body does, and specifically what the lymphatic system does, is it drains and removes that fluid into the system of vessels we call lymph vessels or lymphatic vessels. These lymph vessels essentially connect with larger lymph vessels known as lymphanes. | Lymphatic System .txt |
And that can lead to very serious medical conditions and medical complications. So to prevent this from happening, what our body does, and specifically what the lymphatic system does, is it drains and removes that fluid into the system of vessels we call lymph vessels or lymphatic vessels. These lymph vessels essentially connect with larger lymph vessels known as lymphanes. And along the lymph vessels we have these regions known as lymph nodes. And we'll talk about them in just a moment. And these lymph nodes essentially filter our lymph from different types of pathogenic agents. | Lymphatic System .txt |
And along the lymph vessels we have these regions known as lymph nodes. And we'll talk about them in just a moment. And these lymph nodes essentially filter our lymph from different types of pathogenic agents. And eventually that lymph is returned back into our blood system via specific types of veins, as we'll see in just a moment. And the reason we want to return our lymph back into our blood is because we want to ensure that the same volume of blood remains in our cardiovascular system. So once again, the question is what happens to the 10% fluid that remains in the tissue space? | Lymphatic System .txt |
And eventually that lymph is returned back into our blood system via specific types of veins, as we'll see in just a moment. And the reason we want to return our lymph back into our blood is because we want to ensure that the same volume of blood remains in our cardiovascular system. So once again, the question is what happens to the 10% fluid that remains in the tissue space? If it remains in the tissue space, it will lead to a continual buildup, the process of swelling, the process of edema. And to prevent this from happening, our body uses lymph vessels, shown in green, to drain this fluid out of the interstitial space. Now, the fluid, which is now known as lymph, travels along these venues, along these vessels and eventually connects with these larger vessels we call lymph veins. | Lymphatic System .txt |
If it remains in the tissue space, it will lead to a continual buildup, the process of swelling, the process of edema. And to prevent this from happening, our body uses lymph vessels, shown in green, to drain this fluid out of the interstitial space. Now, the fluid, which is now known as lymph, travels along these venues, along these vessels and eventually connects with these larger vessels we call lymph veins. And eventually the lymph veins reconnect with the blood vessels and the fluid is returned back into our blood circulation through the thoracic duct and the right lymphatic duct that bolt contains that bolt connects with special types of veins. So to see what we mean, let's take a look at the following diagram. So we have two important types of ducts the thoracic duct as well as our right lymphatic duct. | Lymphatic System .txt |
And eventually the lymph veins reconnect with the blood vessels and the fluid is returned back into our blood circulation through the thoracic duct and the right lymphatic duct that bolt contains that bolt connects with special types of veins. So to see what we mean, let's take a look at the following diagram. So we have two important types of ducts the thoracic duct as well as our right lymphatic duct. The thoracic duct essentially collects the lymph from the lower right part of the body, from the GI system and from the left side of the body, the entire left side of the body. And it connects with our circulation system via the left subclavian vein. So this is the bronchiocephalic vein, this is the right subclavian vein and this is the left subclavian vein. | Lymphatic System .txt |
The thoracic duct essentially collects the lymph from the lower right part of the body, from the GI system and from the left side of the body, the entire left side of the body. And it connects with our circulation system via the left subclavian vein. So this is the bronchiocephalic vein, this is the right subclavian vein and this is the left subclavian vein. Remember, the subclavian veins carries the deoxynated blood from the arm portion and into the vena cava which brings that blood to the right atrium of our body. And along the right subclavian vein, we have a connection between that vein and the right lymphatic duct. While along this left subclavian vein we have a connection between this thoracic duct and the left subclavian vein. | Lymphatic System .txt |
Remember, the subclavian veins carries the deoxynated blood from the arm portion and into the vena cava which brings that blood to the right atrium of our body. And along the right subclavian vein, we have a connection between that vein and the right lymphatic duct. While along this left subclavian vein we have a connection between this thoracic duct and the left subclavian vein. So the lymph, once we actually filter that lymph, it returns back into the vein system, bare body and back into the cardiovascular system. So we see that the Rice lymphatic dust collects the lymph from the right side of the head, the necks and the chest and empties into the right subclavian vein. Now, previously we mentioned that one of the other functions of the lymphatic system is to filter our blood, to filter our lymph that travels along these lymph vessels. | Lymphatic System .txt |
So the lymph, once we actually filter that lymph, it returns back into the vein system, bare body and back into the cardiovascular system. So we see that the Rice lymphatic dust collects the lymph from the right side of the head, the necks and the chest and empties into the right subclavian vein. Now, previously we mentioned that one of the other functions of the lymphatic system is to filter our blood, to filter our lymph that travels along these lymph vessels. And this filtering process takes place in lymph nodes. So along many parts of our lymphatic system are small masses of tissue called lymph nodes. So this is one lymph node, a second lymph node, a third lymph node. | Lymphatic System .txt |
And this filtering process takes place in lymph nodes. So along many parts of our lymphatic system are small masses of tissue called lymph nodes. So this is one lymph node, a second lymph node, a third lymph node. And we have many of these lymph nodes along different regions of our body. Now, within these lymph nodes, we have cavities, we have sinuses. And within these cavities, we have specialized types of leukocides wide blood cells. | Lymphatic System .txt |
And we have many of these lymph nodes along different regions of our body. Now, within these lymph nodes, we have cavities, we have sinuses. And within these cavities, we have specialized types of leukocides wide blood cells. Now, when dendritic cells found in the tissue pick up pathogenic antigens, they carry these pathogenic antigens into our lymph nodes. And inside the lymph nodes, we have plasma cells that produce antibodies against these antigens. And these antibodies basically leave the lymph nodes along the other side and eventually, they are dumped into our vein system. | Lymphatic System .txt |
Now, when dendritic cells found in the tissue pick up pathogenic antigens, they carry these pathogenic antigens into our lymph nodes. And inside the lymph nodes, we have plasma cells that produce antibodies against these antigens. And these antibodies basically leave the lymph nodes along the other side and eventually, they are dumped into our vein system. And that's how antibodies end up in the cardiovascular system, in the blood vessels of our body. Now, within these lymph nodes, we also have other wide blood cells, such as macrophages that can engulf any type of pathogenic agent that might be present inside our lymph system. And in this manner, our lymphatic system not only drains our tissue and prevents the build up of fluid inside the tissue, but it also filters our blood. | Lymphatic System .txt |
And that's how antibodies end up in the cardiovascular system, in the blood vessels of our body. Now, within these lymph nodes, we also have other wide blood cells, such as macrophages that can engulf any type of pathogenic agent that might be present inside our lymph system. And in this manner, our lymphatic system not only drains our tissue and prevents the build up of fluid inside the tissue, but it also filters our blood. It basically eats up and digests different types of pathogens that are found inside our blood inside these specialized masses of tissue we call lymph nodes. Now, the final portion that I'd like to focus on is how that fluid actually gets into these lymph vessels in the first place and how the limb travels along our limb vessels. So let's take a look at the following diagram. | Lymphatic System .txt |
It basically eats up and digests different types of pathogens that are found inside our blood inside these specialized masses of tissue we call lymph nodes. Now, the final portion that I'd like to focus on is how that fluid actually gets into these lymph vessels in the first place and how the limb travels along our limb vessels. So let's take a look at the following diagram. So this is a small portion of our lymph vessel. Now, notice along the lymph vessel, we have these endothelial cells. So the walls of the lymph vessels consist of endothelial cells that overlap slightly. | Lymphatic System .txt |
So this is a small portion of our lymph vessel. Now, notice along the lymph vessel, we have these endothelial cells. So the walls of the lymph vessels consist of endothelial cells that overlap slightly. And at the portions where they overlap, these overlapping portions act as one way doors. And when there is a fluid build up inside the tissue, that fluid pressure pushes on these overlapping sections, these one way doors. And that opens these endothelial cells and allows fluid to actually flow into the endothelial cell. | Lymphatic System .txt |
And at the portions where they overlap, these overlapping portions act as one way doors. And when there is a fluid build up inside the tissue, that fluid pressure pushes on these overlapping sections, these one way doors. And that opens these endothelial cells and allows fluid to actually flow into the endothelial cell. So for example, let's imagine that we have a build up of pressure here. And so the fluid pushes against the overlapping portion and the fluid moves into this cavity, this region of our lymph vessel. Now, as the fluid builds up in the lymph vessel, it pushes back onto this side, the other side of our endothelial cell. | Lymphatic System .txt |
So for example, let's imagine that we have a build up of pressure here. And so the fluid pushes against the overlapping portion and the fluid moves into this cavity, this region of our lymph vessel. Now, as the fluid builds up in the lymph vessel, it pushes back onto this side, the other side of our endothelial cell. And because these endothelial cells open only one way and not the other way, when our hydrostatic pressure pushes on our cells this way, the fluid cannot escape back because these overlapping regions between the cells only open this way and not the other way. And we also have a system of one way valves found along the lymph vessel. So that means these valves also open one way and not the other way. | Lymphatic System .txt |
And because these endothelial cells open only one way and not the other way, when our hydrostatic pressure pushes on our cells this way, the fluid cannot escape back because these overlapping regions between the cells only open this way and not the other way. And we also have a system of one way valves found along the lymph vessel. So that means these valves also open one way and not the other way. So when there is a build up of pressure here, it closes these overlapping regions so that fluid cannot exit that lymph node. It pushes against a valve that opens up and that allows the movement of lymph along our vessel as shown in the following diagram. And if there is a decrease in pressure and it basically wants to move back, it cannot move back because when the fluid tries to move back it forces these valves to actually close. | Lymphatic System .txt |
So when there is a build up of pressure here, it closes these overlapping regions so that fluid cannot exit that lymph node. It pushes against a valve that opens up and that allows the movement of lymph along our vessel as shown in the following diagram. And if there is a decrease in pressure and it basically wants to move back, it cannot move back because when the fluid tries to move back it forces these valves to actually close. And that means we do not have a backflow of lymph inside our lymph system in the same way that we do not have a back flow inside our veins. Remember, the veins also contain this valve system that prevents the movement of our lymph back down that lymph vessel. So the walls of the lymph vessels consist of endothelial cells that overlap slightly when there is a build up of fluid in the interstitial tissue, in the tissue space, that creates fluid pressure that pushes on the cells, this opens up those overlapping regions, forces the fluid into that lymph vessel. | Lymphatic System .txt |
And that means we do not have a backflow of lymph inside our lymph system in the same way that we do not have a back flow inside our veins. Remember, the veins also contain this valve system that prevents the movement of our lymph back down that lymph vessel. So the walls of the lymph vessels consist of endothelial cells that overlap slightly when there is a build up of fluid in the interstitial tissue, in the tissue space, that creates fluid pressure that pushes on the cells, this opens up those overlapping regions, forces the fluid into that lymph vessel. Now, inside the lymph vessel we have a system of one wave valves. These valves, as well as the overlapping portion of the endothelial cells open only in one direction and not the other. And this keeps the lymph inside that lymph vessel and it keeps it moving along one direction. | Lymphatic System .txt |
So inside our body we have many different types of glycoproteins and generally speaking, glycoproteins have a wide range of function. So what I'd like to do in this lecture is focus on several important glycoproteins that exist inside our body and see how by adding the sugar component onto the protein, we give the protein the ability to carry out some specific type of process. Now at the end of the lecture I'd also like to discuss an example of a disease known as the eye cell disease that exists in humans that basically demonstrates the importance of protein glycosylation. So let's begin by discussing a category of glycoproteins known as mucins. Now mucins, as we'll see in just a moment, are the major constituents, the major components of the mucus membranes that exist inside our body. So the mucous membranes can be found in the nasal cavity, in our air passageways, the bronchioles and so forth. | Functions of Glycoproteins and I-Cell Disease .txt |
So let's begin by discussing a category of glycoproteins known as mucins. Now mucins, as we'll see in just a moment, are the major constituents, the major components of the mucus membranes that exist inside our body. So the mucous membranes can be found in the nasal cavity, in our air passageways, the bronchioles and so forth. Now mucints are basically these heavily glycosylated proteins that are produced and released by the epithelial tissue, the epithelial cells of our body. Now heavily glycosylated basically means there are many oligosaccharides, many sugar molecules found attached onto these proteins. The reason, the question is why? | Functions of Glycoproteins and I-Cell Disease .txt |
Now mucints are basically these heavily glycosylated proteins that are produced and released by the epithelial tissue, the epithelial cells of our body. Now heavily glycosylated basically means there are many oligosaccharides, many sugar molecules found attached onto these proteins. The reason, the question is why? Well, if we examine the protein sequence, the amino acid sequence of the protein will find a high density, a high number of serene and three ending residues. And it's these two residues that are basically needed to produce the old glycocytic bonds between the protein and the sugar molecule. So because mucins contain a high number of threeanine and steam residues, they are heavily glycosylated with the old glycositic linkages. | Functions of Glycoproteins and I-Cell Disease .txt |
Well, if we examine the protein sequence, the amino acid sequence of the protein will find a high density, a high number of serene and three ending residues. And it's these two residues that are basically needed to produce the old glycocytic bonds between the protein and the sugar molecule. So because mucins contain a high number of threeanine and steam residues, they are heavily glycosylated with the old glycositic linkages. Now, although most mucins are actually produced by the cells and released into the extracellular matrix, some of these mucins actually remain attached onto the cell membrane. And this is what is shown in this diagram. So we have the cell membrane, we have this hydrophobic section of the protein Children Brown and this is the rest of that protein. | Functions of Glycoproteins and I-Cell Disease .txt |
Now, although most mucins are actually produced by the cells and released into the extracellular matrix, some of these mucins actually remain attached onto the cell membrane. And this is what is shown in this diagram. So we have the cell membrane, we have this hydrophobic section of the protein Children Brown and this is the rest of that protein. And these are basically the ligosaccharides. And we have many of these oligosaccharides as shown. So what exactly is a function of mucins? | Functions of Glycoproteins and I-Cell Disease .txt |
And these are basically the ligosaccharides. And we have many of these oligosaccharides as shown. So what exactly is a function of mucins? Well, because mucins are part of the mucus membrane and the mucus membrane basically acts to lubricate and protect our body from pathogenic agents. What that means is these individual mucins have to be able to carry out that specific function. Now how exactly does it carry out the function of lubrication? | Functions of Glycoproteins and I-Cell Disease .txt |
Well, because mucins are part of the mucus membrane and the mucus membrane basically acts to lubricate and protect our body from pathogenic agents. What that means is these individual mucins have to be able to carry out that specific function. Now how exactly does it carry out the function of lubrication? Well, basically these red oligosaccharides contain modified sugar molecules that contain negative charges and these negative charges attract water molecules which are polar molecules. And so as a result of those charges we're basically going to have many of these water molecules which are basically going to surround this entire mucin molecule. And as a result that basically gives the addition of these sugar molecules, gives the mucins, these proteins, the ability to actually absorb water. | Functions of Glycoproteins and I-Cell Disease .txt |
Well, basically these red oligosaccharides contain modified sugar molecules that contain negative charges and these negative charges attract water molecules which are polar molecules. And so as a result of those charges we're basically going to have many of these water molecules which are basically going to surround this entire mucin molecule. And as a result that basically gives the addition of these sugar molecules, gives the mucins, these proteins, the ability to actually absorb water. And that's exactly what gives the mucous membranes the ability to lubricate those epithelial cells. On top of that, these carbohydrates are very sticky and they can basically trap pathogenic and infectious agents. And so that means the mucints that form the mucus barriers basically have the ability to lubricate and protect epithelial tissue. | Functions of Glycoproteins and I-Cell Disease .txt |
And that's exactly what gives the mucous membranes the ability to lubricate those epithelial cells. On top of that, these carbohydrates are very sticky and they can basically trap pathogenic and infectious agents. And so that means the mucints that form the mucus barriers basically have the ability to lubricate and protect epithelial tissue. Now, let's move on to the second type of glycoprotein that we'll find inside our body. And this is known as erythropoietin, or EPO. Now, urethropoietin is a glycoprotein, and the protein component basically consists of an amino acid sequence of 165 amino acids. | Functions of Glycoproteins and I-Cell Disease .txt |
Now, let's move on to the second type of glycoprotein that we'll find inside our body. And this is known as erythropoietin, or EPO. Now, urethropoietin is a glycoprotein, and the protein component basically consists of an amino acid sequence of 165 amino acids. And four of these amino acids are actually glycosylated. So three of these amino acids are asparaging amino acids, and that means we have the N glycocitic bonds, and one of these amino acids is the Serene amino acid, and that means we have the O glycocitic bond. And so this brown section, which actually looks like a bunny, this brown section is the protein component of erythropolietin. | Functions of Glycoproteins and I-Cell Disease .txt |
And four of these amino acids are actually glycosylated. So three of these amino acids are asparaging amino acids, and that means we have the N glycocitic bonds, and one of these amino acids is the Serene amino acid, and that means we have the O glycocitic bond. And so this brown section, which actually looks like a bunny, this brown section is the protein component of erythropolietin. And these are these four oligosaccharides, which are bound onto these four different amino acids. Three of them are asparagus, three of them are asparagine, and one of them is the serene. Now, what exactly is the function of erythropletin? | Functions of Glycoproteins and I-Cell Disease .txt |
And these are these four oligosaccharides, which are bound onto these four different amino acids. Three of them are asparagus, three of them are asparagine, and one of them is the serene. Now, what exactly is the function of erythropletin? Well, erythropletin is basically a glycoprotein that is produced by special cells found inside our kidneys. And these glycoproteins are released into the blood plasma and they act as hormones. They basically bind on suspension precursor cells and they stimulate the cells to basically produce erythrocytes, red blood cells. | Functions of Glycoproteins and I-Cell Disease .txt |
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