Steroid hormone synthesis pathway Human ovary diagram

Androgen Receptor Pathway | Androgen Receptor …

Pathway Central: Estrogen Pathway - SABiosciences

This has led to the development of a number of novel agents targeting the AR signaling pathway, including more effective antiandrogens, inhibitors of CYP17, an enzyme required for androgen synthesis, inhibitors of 5α-reductase, inhibitors of HSP90 which protects AR from degradation, inhibitors of histone deacetylases which is required for optimal AR-mediated transcription, as well as inhibitors of tyrosine kinase inhibitors.

Androgen deprivation therapy - Wikipedia

Pathway Central: Akt Signaling - SABiosciences

AB - Recently, dihydrotestosterone biosynthesis through the backdoor pathway has been implicated for the human testis in addition to the classic pathway for testosterone (T) synthesis. In the human ovary, androgen precursors are crucial for estrogen synthesis and hyperandrogenism in pathologies such as the polycystic ovary syndrome is partially due to ovarian overproduction. However, a role for the backdoor pathway is only established for the testis and the adrenal, but not for the human ovary. To investigate whether the backdoor pathway exists in normal and PCOS ovaries, we performed specific gene and protein expression studies on ovarian tissues. We found aldo-keto reductases (AKR1C1-1C4), 5α-reductases (SRD5A1/2) and retinol dehydrogenase (RoDH) expressed in the human ovary, indicating that the ovary might produce dihydrotestosterone via the backdoor pathway. Immunohistochemical studies showed specific localization of these proteins to the theca cells. PCOS ovaries show enhanced expression, what may account for the hyperandrogenism.

MK-2866 (GTx-024) | Androgen Receptor modulator | …

Recently, dihydrotestosterone biosynthesis through the backdoor pathway has been implicated for the human testis in addition to the classic pathway for testosterone (T) synthesis. In the human ovary, androgen precursors are crucial for estrogen synthesis and hyperandrogenism in pathologies such as the polycystic ovary syndrome is partially due to ovarian overproduction. However, a role for the backdoor pathway is only established for the testis and the adrenal, but not for the human ovary. To investigate whether the backdoor pathway exists in normal and PCOS ovaries, we performed specific gene and protein expression studies on ovarian tissues. We found aldo-keto reductases (AKR1C1-1C4), 5α-reductases (SRD5A1/2) and retinol dehydrogenase (RoDH) expressed in the human ovary, indicating that the ovary might produce dihydrotestosterone via the backdoor pathway. Immunohistochemical studies showed specific localization of these proteins to the theca cells. PCOS ovaries show enhanced expression, what may account for the hyperandrogenism.

What is AIS? - Androgen Insensitivity Syndrome …


Peptide Hormones - The Medical Biochemistry Page

The two mammalian ERs exhibit modular structures characteristic of the nuclear receptor superfamily. They are composed of three independent but interacting functional domains: the NH2-terminal transcriptional AF1 (Activation Function-1) domain, the DNA-binding domain, and the ligand-binding domain that contains a ligand-dependent transcriptional AF2 (Activation Function-2) domain (Ref.3). ERs integrate multiple signals both from ligands and intracellular signalling pathways to perform their functions in the nucleus and cytosol. The vasculature (like the reproductive tissue, bone, liver, and brain) has been recognized as an important target of estrogen action through rapid nongenomic effects and/or via the classic pathway (genomic effects) involving ERs (Ref.4). The classical pathways depend on direct interaction of estrogen with its receptor in the nucleus. Once activated, the ER complex can directly mediate gene transcription or interact with transcription factors to influence their activity. The nonclassical pathways work more rapidly and depend on the ability of estrogen to interact with either nonsteroid hormone receptors or steroid hormone receptors in the membrane. Both nonclassical pathways activate kinases that ultimately regulate transcription of specific genes (Ref.5).