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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Leydig cell aging: Molecular mechanisms and treatments
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<blockquote data-quote="madman" data-source="post: 209085" data-attributes="member: 13851"><p><strong>Fig. 2 <u>SITE formation driving cholesterol import into mitochondria</u>. Cholesterol import into mitochondria is the result of series of protein-protein interactions. <u>The involved proteins include</u>: (<u>A</u>) cytosolic proteins ACBD1, ACBD3, Sec23ip, PKARIα, STARD1, and 14-3-3 adaptor proteins, 14-3-3γ and 14-3-3ε (<u>red</u>); (<u>B</u>) OMM proteins TSPO, VDAC and ATAD3 (<u>blue</u>); and (<u>c</u>) IMM proteins CYP11A1, ADX-adrenodoxin and ADR-adrenodoxin reductase (<u>green</u>). ACBD1/DBI is a TSPO endogenous ligand. The TSPO and VDAC complex located at the contact sites between outer and inner mitochondrial membranes recruits ACBD3 protein, a PKA anchoring protein, to mitochondria. The hormone-induced STARD1 protein is targeted to OMM where it interacts with VDAC and is locally phosphorylated by PKA for maximal activity. 14-3-3 adaptor proteins, binding to either STAR (14-3-3γ) or VDAC1 (14-3-3ε), provide negative control of steroid formation, thus allowing for sustainable steroid formation. Sec23pi binds to and controls 14-3-3γ activity. The formation of SITE allows for the translocation of cholesterol directly across mitochondrial membranes and intermembrane space to CYP11A1 for metabolism. In aged Leydig cells, the levels of TSPO, STARD1, and CYP11A1 are reduced.</strong></p><p><strong>[ATTACH=full]16796[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 209085, member: 13851"] [B]Fig. 2 [U]SITE formation driving cholesterol import into mitochondria[/U]. Cholesterol import into mitochondria is the result of series of protein-protein interactions. [U]The involved proteins include[/U]: ([U]A[/U]) cytosolic proteins ACBD1, ACBD3, Sec23ip, PKARIα, STARD1, and 14-3-3 adaptor proteins, 14-3-3γ and 14-3-3ε ([U]red[/U]); ([U]B[/U]) OMM proteins TSPO, VDAC and ATAD3 ([U]blue[/U]); and ([U]c[/U]) IMM proteins CYP11A1, ADX-adrenodoxin and ADR-adrenodoxin reductase ([U]green[/U]). ACBD1/DBI is a TSPO endogenous ligand. The TSPO and VDAC complex located at the contact sites between outer and inner mitochondrial membranes recruits ACBD3 protein, a PKA anchoring protein, to mitochondria. The hormone-induced STARD1 protein is targeted to OMM where it interacts with VDAC and is locally phosphorylated by PKA for maximal activity. 14-3-3 adaptor proteins, binding to either STAR (14-3-3γ) or VDAC1 (14-3-3ε), provide negative control of steroid formation, thus allowing for sustainable steroid formation. Sec23pi binds to and controls 14-3-3γ activity. The formation of SITE allows for the translocation of cholesterol directly across mitochondrial membranes and intermembrane space to CYP11A1 for metabolism. In aged Leydig cells, the levels of TSPO, STARD1, and CYP11A1 are reduced. [ATTACH type="full"]16796[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Leydig cell aging: Molecular mechanisms and treatments
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