Abstract
Δ113p53/Δ133p53: survival and integrity.
Highlights
In 2005, two reports, one on analysis of 5’-RACE PCR products of p53 transcripts in human normal tissues [1] and the other on analysis of a zebrafish genetic mutant defhi429 [2], described the discovery of p53 isoforms
DNA double strand breaks (DSB) are the most deleterious DNA lesions that a cell can encounter. To combat these detrimental insults, three pathways have evolved for the repair of DSB: Homologous Recombination (HR), Non-Homologous End Joining (NHEJ) and Single-Strand Annealing (SSA)
It is well established that full-length p53 represses DNA DSB repair by either preventing repair complex formation through interacting with several essential HR-related proteins such as RAD51 and RPA, or transcriptionally suppressing the expression of DNA DSB repair genes e.g. RAD51, RECQ4 and WRN [7]
Summary
In 2005, two reports, one on analysis of 5’-RACE PCR products of p53 transcripts in human normal tissues [1] and the other on analysis of a zebrafish genetic mutant defhi429 [2], described the discovery of p53 isoforms. It is well established that full-length p53 represses DNA DSB repair by either preventing repair complex formation through interacting with several essential HR-related proteins such as RAD51 and RPA, or transcriptionally suppressing the expression of DNA DSB repair genes e.g. RAD51, RECQ4 and WRN [7]. This is consistent with the observation that p53 protein is rapidly accumulated to a high level in response to DNA DSB stress at early stage.
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