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The thyroid hormone receptor (TR) [1] is a type of nuclear receptor that is activated by binding thyroid hormone. [2] TRs act as transcription factors , ultimately affecting the regulation of gene transcription and translation .
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.
Mechanism of class II nuclear receptor action. A class II nuclear receptor (NR), regardless of ligand-binding status, is located in the nucleus bound to DNA. For the purpose of illustration, the nuclear receptor shown here is the thyroid hormone receptor heterodimerized to the RXR.
Thyroid hormone receptor beta (TR-beta) also known as nuclear receptor subfamily 1, group A, member 2 (NR1A2), is a nuclear receptor protein that in humans is encoded by the THRB gene. [ 5 ] [ 6 ] Function
A hormone receptor is a receptor molecule that binds to a specific hormone. Hormone receptors are a wide family of proteins made up of receptors for thyroid and steroid hormones, retinoids and Vitamin D, and a variety of other receptors for various ligands, such as fatty acids and prostaglandins. [1] Hormone receptors are of mainly two classes.
Thyroid hormones act by crossing the cell membrane and binding to intracellular nuclear thyroid hormone receptors TR-α 1, TR-α 2, TR-β 1, and TR-β 2, which bind with hormone response elements and transcription factors to modulate DNA transcription.
Thyroid-stimulating hormone (TSH) released from the anterior pituitary gland binds the TSH receptor (a G s protein-coupled receptor) on the basolateral membrane of the cell and stimulates the endocytosis of the colloid. The endocytosed vesicles fuse with the lysosomes of the follicular cell.
The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland.