Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2006 Sep;8(9):1025-31.
doi: 10.1038/ncb1468. Epub 2006 Aug 6.

Interactions between E2F1 and SirT1 regulate apoptotic response to DNA damage

Chuangui Wang  1 , Lihong Chen, Xinghua Hou, Zhenyu Li, Neha Kabra, Yihong Ma, Shino Nemoto, Toren Finkel, Wei Gu, W Douglas Cress, Jiandong Chen
Affiliations

Interactions between E2F1 and SirT1 regulate apoptotic response to DNA damage

Chuangui Wang et al. Nat Cell Biol. 2006 Sep.

Abstract

The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sir2 (silent information regulator 2) regulates gene silencing in yeast and promotes lifespan extension during caloric restriction. The mammalian homologue of Sir2 (SirT1) regulates p53, NF-kappaB and Forkhead transcription factors, and is implicated in stress response. This report shows that the cell-cycle and apoptosis regulator E2F1 induces SirT1 expression at the transcriptional level. Furthermore, SirT1 binds to E2F1 and inhibits E2F1 activities, forming a negative feedback loop. Knockdown of SirT1 by small interference RNA (siRNA) increases E2F1 transcriptional and apoptotic functions. DNA damage by etoposide causes E2F1-dependent induction of SirT1 expression and knockdown of SirT1 increases sensitivity to etoposide. These results reveal a mutual regulation between E2F1 and SirT1 that affects cellular sensitivity to DNA damage.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

  NODES
Project 1
twitter 2