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Increasing cyclin D1 levels during the G1 phase is induced by mitogenic growth factors [25] primarily through Ras mediated pathways, [26] [27] [28] and hormones. [22] These Ras-mediated pathways lead to the increase in transcription of cyclin D1, and inhibit its proteolysis and export from the nucleus. [29] Cyclin D1 is degraded via an ubiquitin-mediated proteolysis pathway at the end of the S-phase. Phosphorylation of cyclin D1’s threonine residue T286 marks the protein for export from the nucleus and proteolytic degradation. [30]

Progestogens The discovery that ethinyl substitution leads to oral potency led to the preparation of ethisterone, an orally active derivative of testosterone. In 1951, it was found that removal of the carbon-19 from ethisterone to form norethindrone did not destroy the oral activity and, most importantly, changed the major hormonal effect from that of an androgen to that of a progestogen. Accordingly, the progestational derivatives of testosterone were designated 19-nortestosterones. The androgenic properties of these compounds, however, were not completely eliminated, and minimal anabolic and androgenic activity remains. Examples of this class of progestogens include norethindrone, norethynodrel, ethynodiol diacetate, and some other related compounds not used in the United States. The second group of 19-nor compounds are gonanes, which have an 18-ethyl instead of an 18-methyl group. They include racemic norgestrel, levonorgestrel, and three newer compounds: gestodene, desogestrel (a pro-drug that must be converted to 3-ketodesogestrel to be biologically active) and norgestimate, which is the 17-acetyl-3-oxime derivative of norgestrel, into which it is rapidly metabolized.

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