By the same authors

From the same journal

SIRT3 is pro-apoptotic and participates in distinct basal apoptotic pathways

Research output: Contribution to journalArticle

Author(s)

Department/unit(s)

Publication details

JournalCell cycle
DatePublished - 1 Nov 2007
Issue number21
Volume6
Number of pages9
Pages (from-to)2669-2677
Original languageEnglish

Abstract

SIRT3, one of seven mammalian sirtuins, is a NAD-dependent deacetylase. SIRT3 localizes to mitochondria where it deacetylates and thus activates acetyl-CoA synthetase 2 (AceCS2), indicating a role for SIRT3 in metabolism. Here we provide evidence that SIRT3 also impacts upon apoptosis and cell growth control. Using RNAi under basal (non-stress) conditions we show that SIRT3 is required for apoptosis induced by selective silencing of Bcl-2 in HCT116 human epithelial cancer cells. Identical treatment of ARPE19 epithelial non-cancer cells induces G(1) growth arrest which also proved to be SIRT3-dependent. Previously we have identified SIRT1 and JNK2 as constitutive suppressors of apoptosis in HCT116 cells. We now demonstrate that SIRT3 functions in JNK2-regulated apoptosis but is dispensable for SIRT1-regulated apoptosis. SIRT3 is also dispensable for stress-induced apoptosis. Thus the pro-apoptotic functioning of SIRT3 is selectively coupled with defined pathways regulating cell survival under basal conditions.

    Research areas

  • SIRT3, apoptosis, growth arrest, cancer, non-cancer, DEPENDENT DEACETYLASE, TRANSCRIPTION FACTORS, HISTONE DEACETYLASE, CALORIE RESTRICTION, CELL-SURVIVAL, DNA-DAMAGE, P53, MITOCHONDRIA, HOMOLOG, SIRTUINS

Discover related content

Find related publications, people, projects, datasets and more using interactive charts.

View graph of relations