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Because the receptor gene is expressed in several forms, it has many different (pleiotropic) effects in different parts of the body. When glucocorticoids bind to GR, its primary mechanism of action is the regulation of gene transcription. [5] [6] The unbound receptor resides in the cytosol of the cell. After the receptor is bound to ...
Cortisol is a steroid hormone in the glucocorticoid class of hormones and a stress hormone.When used as medication, it is known as hydrocortisone.. It is produced in many animals, mainly by the zona fasciculata of the adrenal cortex in an adrenal gland. [1]
This gene encodes a transcriptional repressor which represses neuronal genes in non-neuronal tissues. It is a member of the Kruppel -type zinc finger transcription factor family. It represses transcription by binding a DNA sequence element called the neuron-restrictive silencer element (NRSE, also known as RE1).
The goal is to normalize the production of 21-hydroxylase, the enzyme encoded by CYP21A2. Providing a working copy of this gene may improve adrenal hormone synthesis and subsequently normalize cortisol and aldosterone production. [253] Currently, gene replacement therapy for CAH is still at an early stage of research and development.
However, in humans, cortisol is the primary glucocorticoid that is produced primarily in the zona fasciculata of the adrenal cortex. Corticosterone has only weak glucocorticoid and mineralocorticoid potencies in humans and is important mainly as an intermediate in the steroidogenic pathway from pregnenolone to aldosterone.
In addition, the encoded protein can catalyze the reverse reaction, the conversion of cortisone to cortisol. Too much cortisol can lead to central obesity, and a particular variation in this gene has been associated with obesity and insulin resistance in children. Two transcript variants encoding the same protein have been found for this gene.
Individuals who have generalized glucocorticoid resistance may exhibit biochemical hypercortisolism in the absence of Cushing's syndrome symptoms. [6] The condition's clinical phenotype varies from cases with no symptoms to signs of excess mineralocorticoids in the body such as hypokalemic alkalosis and hypertension and/or androgen excess, including oligospermia in males, menstrual ...
This gene encodes an alpha-globulin protein with corticosteroid-binding properties. This is the major transport protein for glucocorticoids and progestins in the blood of most vertebrates. The gene localizes to a chromosomal region containing several closely related serine protease inhibitors ( serpins ).