Abstract
Bcl-2 has previously been characterized as an anti-apoptotic protein. However, it has now been linked to DNA mismatch repair (MMR). By retaining E2F-1 in a transcriptionally inactive state, through the induction of hypophosphorylated retinoblastoma protein, Bcl-2 hinders the expression of a key component of mismatch repair, MSH2. This study could therefore help to explain the mutagenicity that is associated with Bcl-2.
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