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Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
The role of androgen therapy in prostate cancer: from TRT to BAT
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<blockquote data-quote="madman" data-source="post: 195998" data-attributes="member: 13851"><p><strong>FIGURE 1 Potential mechanism of prostate cancer growth inhibition through high doses of androgen. (a) In the presence of high doses of androgen (pink spheres), androgen signaling leads to recruitment of AR (light purple squares) and TOP2b. TOP2b-mediated DNA DSBs in the regulatory regions of AR target genes results in DNA damage and cell apoptosis. (b) Activation of AR occurs at certain ARBSs and acts as a transcriptional repressor through the recruitment of LSD1 and the demethylation of activating histone marks (H3K4me1 and H3K4me2), resulting in reduced expression of full-length AR and the generation of spliced variants. (c) Under the condition of high doses of androgen, activated AR binds to the protein ORS. Ligand-dependent stabilization of AR during mitosis might inhibit the Q1 degradation of AR in M phase, preventing re-licensing for DNA replication during G1, resulting in S-phase arrest.</strong></p><p><strong>[ATTACH=full]12953[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 195998, member: 13851"] [B]FIGURE 1 Potential mechanism of prostate cancer growth inhibition through high doses of androgen. (a) In the presence of high doses of androgen (pink spheres), androgen signaling leads to recruitment of AR (light purple squares) and TOP2b. TOP2b-mediated DNA DSBs in the regulatory regions of AR target genes results in DNA damage and cell apoptosis. (b) Activation of AR occurs at certain ARBSs and acts as a transcriptional repressor through the recruitment of LSD1 and the demethylation of activating histone marks (H3K4me1 and H3K4me2), resulting in reduced expression of full-length AR and the generation of spliced variants. (c) Under the condition of high doses of androgen, activated AR binds to the protein ORS. Ligand-dependent stabilization of AR during mitosis might inhibit the Q1 degradation of AR in M phase, preventing re-licensing for DNA replication during G1, resulting in S-phase arrest. [ATTACH type="full"]12953[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
The role of androgen therapy in prostate cancer: from TRT to BAT
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