Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8475224 | Journal of Molecular and Cellular Cardiology | 2013 | 8 Pages |
Abstract
Working model for the mechanism by which testosterone enhances cardiomyogenesis in stem cells. Testosterone and its active metabolite DHT are known to bind to AR-1 and translocate into the nucleus (gray arrows). During testosterone-enhanced cardiomyogenesis, formation of the AR1/testosterone complex is essential (black inhibitory arrows) for binding to the MEF2C and HCN4 genes (black arrow). This would lead to enhanced H3K14 acetylation and upregulated transcription of MEF2C, HCN4, leading to cardiomyogenesis, likely in collaboration with other cardiomyogenic transcription factors (CTF).118
Keywords
nIFChIP-qPCRMLC2vCa2 +/calmodulin-dependent protein kinaseH3K14acMyocyte enhancer factor 2CDHPRCACNA1SBicalutamideHCN4MEF2CCTFANFAREsCaMKDHTqPCRBICchromatin immunoprecipitationembryoid bodyDihydrotestosteroneMyosin heavy chainMouse embryonic stem cellsAndrogen response elementsatrial natriuretic factorFinasterideMHCMeSNifedipinefinCHiPEmbryonal carcinomadihydropyridine receptorAndrogen Receptor
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Authors
Ashraf Said Al Madhoun, Anastassia Voronova, Tammy Ryan, Abeer Zakariyah, Christian McIntire, Laura Gibson, Michael Shelton, Marc Ruel, Ilona S. Skerjanc,