Author: ["Cha-Kyung Youn","Hyun-Ju Cho","Soo-Hyun Kim","Hong-Beum Kim","Mi-Hwa Kim","In-Youb Chang","Jung-Sup Lee","Myung-Hee Chung","Kyung-Soo Hahm","Ho Jin You"]
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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.Cite this article
Youn, CK., Cho, HJ., Kim, SH. et al. Bcl-2 expression suppresses mismatch repair activity through inhibition of E2F transcriptional activity. Nat Cell Biol 7, 137–147 (2005). https://doi.org/10.1038/ncb1215 