Steroid hormones bind to receptors inside the cell

The mineralocorticoid pathway starts with 21-hydroxylation of progesterone to form deoxycorticosterone (DOC). The enzyme in this reaction, 21-hydroxylase, is encoded by the CYP21 gene. 11 , 12 Deoxycorticosterone is then converted to corticosterone through the action of 11β-hydroxylase. There are two distinct 11β-hydroxylase isoenzymes, both of which are encoded by two genes, CYP11B1 and CYP11B2 . 13 Corticosterone is hydroxylated at carbon 18 to form 18-hydroxycorticosterone, which is transformed to aldosterone by removal of two hydrogens (oxidation) at carbon 18. These two reactions are catalyzed by 18-hydroxylase and 18-hydroxysteroid dehydrogenase, respectively, which are encoded by the same gene, CYP11B2 . Transcription of CYP11B1 is regulated primarily by ACTH, whereas angiotensin II regulates CYP11B2 transcription. 14 , 15 Similarly, the glucocorticoid pathway begins with 17α-hydroxyprogesterone, which is converted to deoxycortisol and subsequently to cortisol by 21-hydroxylase and 11β-hydroxylase, respectively, in the same manner as the conversion of progesterone to corticosterone. A deficiency of 21-hydroxylase, 11β-hydroxylase, or 3β-HSD in the adrenals may result in congenital adrenal hyperplasia and female pseudohermaphroditism, manifested as a masculinized female fetus.

The formation of the corpus luteum (which produces the majority of progesterone) is triggered by a surge in luteinising hormone production by the anterior pituitary gland . This normally occurs at approximately day 14 of the menstrual cycle and it stimulates the release of an egg from the ovary and the formation of the corpus luteum. The corpus luteum then releases progesterone, which prepares the body for pregnancy. If the egg is not fertilised and no embryo is conceived, the corpus luteum breaks down and the production of progesterone decreases. As the lining of the womb is no longer maintained by progesterone from the corpus luteum, it breaks away and menstrual bleeding occurs, marking the start of a new menstrual cycle.

The secretion of hypothalamic, pituitary, and target tissue hormones is under tight regulatory control by a series of feedback and feed- forward loops. This complexity can be demonstrated using the growth hormone (GH) regulatory system as an example. The stimulatory substance growth hormone releasing hormone (GHRH) and the inhibitory substance somatostatin (SS) both products of the hypothalamus, control pituitary GH secretion. Somatostatin is also called growth hormone-inhibiting hormone (GHIH). Under the influence of GHRH, growth hormone is released into the systemic circulation, causing the target tissue to secrete insulin-like growth factor-1, IGF-1. Growth hormone also has other more direct metabolic effects; it is both hyperglycemic and lipolytic. The principal source of systemic IGF-1 is the liver, although most other tissues secrete and contribute to systemic IGF-1. Liver IGF-1 is considered to be the principal regulator of tissue growth. In particular, the IGF-1 secreted by the liver is believed to synchronize growth throughout the body, resulting in a homeostatic balance of tissue size and mass. IGF-1 secreted by peripheral tissues is generally considered to be autocrine or paracrine in its biological action.

The C-terminal AF-2 transactivation domain is highly conserved within the nuclear receptor superfamily 31 and is recognized by various transcriptional coactivators. 32 , 33 AF-2 is localized to the most C-terminal end of the E domain. A third transactivation domain called AF-2a or tau2 has been localized to the N-terminal region of the LBD of ERα 31 and GR. 34 Deletion experiments revealed a role for AF-2a and the DBD in targeting rat GR to the nuclear matrix, 35 an interconnected ribonuclear-protein network within the nucleus that is thought to play an important roles in transcription of active genes by stabilizing the assembly of the transcriptional machinery. 36

Modern molecular biology has ushered in a new era in endocrine research, where nuclear receptors can be identified and their genes cloned before their hormone ligands are known. In fact, scientists have currently identified the hormone ligand for only about half of the approximately seventy different nuclear receptors that are now known. The receptors for unknown hormone ligands are called orphan receptors. For example, the receptor known as the retinoid X receptor (abbreviated RXR) was an orphan until its ligand, 9-cis-retinoic acid (a vitamin A derivative) was discovered. The significance of this receptor will be described shortly.

Steroid hormones bind to receptors inside the cell

steroid hormones bind to receptors inside the cell

The C-terminal AF-2 transactivation domain is highly conserved within the nuclear receptor superfamily 31 and is recognized by various transcriptional coactivators. 32 , 33 AF-2 is localized to the most C-terminal end of the E domain. A third transactivation domain called AF-2a or tau2 has been localized to the N-terminal region of the LBD of ERα 31 and GR. 34 Deletion experiments revealed a role for AF-2a and the DBD in targeting rat GR to the nuclear matrix, 35 an interconnected ribonuclear-protein network within the nucleus that is thought to play an important roles in transcription of active genes by stabilizing the assembly of the transcriptional machinery. 36

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