Interestingly, our data also revealedthat the deacetylase activity of SIRT1 is not required for E-cadherinrepression, because a catalytically inactive SIRT1 protein (SIRT1-HY) reducedE-cadherin levels as well as wild-type SIRT1 (Fig. 5D, E).These observations, together with our finding that both wild-type and mutantSIRT1 proteins interact equally with SIRT7 (Fig. 5F),suggest that the physical interaction of SIRT1 with SIRT7 is required forSIRT1-dependent transcriptional repression of E-cadherin in prostate carcinomacells. The gene discussed is SIRT1; the disease is prostatitis.