Publications by authors named "Marc A Kerzhnerman"
Although mismatch repair (MMR) is essential for correcting DNA replication errors, it can also recognize other lesions, such as oxidized bases. In G0 and G1, MMR is kept in check through unknown mechanisms as it is error-prone during these cell cycle phases. We show that in mammalian cells, D-type cyclins are recruited to sites of oxidative DNA damage in a PCNA- and p21-dependent manner.
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- * D-type cyclins are recruited to oxidative damage sites, protecting p21 from degradation, which in turn blocks MMR by competing with MMR components for binding to PCNA.
- * The degradation of D-type cyclins at the G1/S transition is crucial for allowing MMR proteins to interact with PCNA, ensuring proper repair of DNA replication errors; however, persistent cyclin D1 during S-phase can increase mutation rates.
DNA has dedicated cellular repair pathways capable of coping with lesions that could arise from both endogenous and/or exogenous sources. DNA repair necessitates collaboration between numerous proteins, responsible for covering a broad range of tasks from recognizing and signaling the presence of a DNA lesion to physically repairing it. During this process, tracks of single-stranded DNA (ssDNA) are often created, which are eventually filled by DNA polymerases.
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