Thyroid hormones
The thyroid hormones function via a well-studied set of nuclear receptors, termed the thyroid hormone receptors. These receptors, together with corepressor molecules, bind DNA regions called thyroid hormone response elements (TREs) near genes. This receptor-corepressor-DNA complex can block gene transcription. Triiodothyronine (T3), which is the active form of thyroxine(T4), goes on to bind to receptors. The deiodinase catalyzed reaction removes an iodine atom from the 5' position of the outer aromatic ring of Thyroxine's (T4) structure. When triiodothyronine (T3) binds a receptor, it induces a conformational change in the receptor, displacing the corepressor from the complex. This leads to recruitment of coactivator proteins and RNA polymerase, activating transcription of the gene.
Thyroid storm
The precise mechanism for the development of thyroid storm is poorly understood. In the human body, thyroid hormone may be free (biologically active T3/T4) or bound to thyroid binding hormone (biologically inactive) to be transported. The release of thyroid hormone is tightly regulated by a feedback system involving the hypothalamus, pituitary gland, and thyroid gland. Hyperthyroidism results from a dysregulation of this system that eventually leads to increases in levels of free T3/T4. The transition from simple hyperthyroidism to the medical emergency of thyroid storm may be triggered by conditions (see Causes) that lead to the following: