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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 
 

Hormonal Control of Androgen Receptor Function through SIRT1.

The NAD-dependent histone deacetylase Sir2 plays a key role in connecting cellular metabolism with gene silencing and aging. The androgen receptor (AR) is a ligand-regulated modular nuclear receptor governing prostate cancer cellular proliferation, differentiation, and apoptosis in response to androgens, including dihydrotestosterone (DHT). Here, SIRT1 antagonists induce endogenous AR expression and enhance DHT-mediated AR expression. SIRT1 binds and deacetylates the AR at a conserved lysine motif. Human SIRT1 (hSIRT1) repression of DHT- induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1. SIRT1 inhibited coactivator- induced interactions between the AR amino and carboxyl termini. DHT-induced prostate cancer cellular contact-independent growth is also blocked by SIRT1, providing a direct functional link between the AR, which is a critical determinant of progression of human prostate cancer, and the sirtuins.[1]

References

  1. Hormonal Control of Androgen Receptor Function through SIRT1. Fu, M., Liu, M., Sauve, A.A., Jiao, X., Zhang, X., Wu, X., Powell, M.J., Yang, T., Gu, W., Avantaggiati, M.L., Pattabiraman, N., Pestell, T.G., Wang, F., Quong, A.A., Wang, C., Pestell, R.G. Mol. Cell. Biol. (2006) [Pubmed]
 
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