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Bcl-2 expression suppresses mismatch repair activity through inhibition of E2F transcriptional activity.

Abstract：

:Bcl-2 stimulates mutagenesis after the exposure of cells to DNA-damaging agents. However, the biological mechanisms of Bcl-2-mediated mutagenesis have remained largely obscure. Here we demonstrate that the Bcl-2-mediated suppression of hMSH2 expression results in a reduced cellular capacity to repair mismatches. The pathway linking Bcl-2 expression to the suppression of mismatch repair (MMR) activity involves the hypophosphorylation of pRb, and then the enhancement of the E2F-pRb complex. This is followed by a decrease in hMSH2 expression. MMR has a key role in protection against deleterious mutation accumulation and in maintaining genomic stability. Therefore, the decreased MMR activity by Bcl-2 may be an underlying mechanism for Bcl-2-promoted oncogenesis.

journal_name

Nat Cell Biol

journal_title

Nature cell biology

authors

Youn CK,Cho HJ,Kim SH,Kim HB,Kim MH,Chang IY,Lee JS,Chung MH,Hahm KS,You HJ

doi

10.1038/ncb1215

keywords:

subject

Has Abstract

pub_date

2005-02-01 00:00:00

pages

137-47

issue

2

eissn

1465-7392

issn

1476-4679

pii

ncb1215

journal_volume

7

pub_type

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