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Tumour suppressors, kinases and clamps: How p53 regulates the cell cycle in response to DNA damage
Author(s) -
Cox Lynne S.,
Lane David P.
Publication year - 1995
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.950170606
Subject(s) - dna damage , cell cycle , biology , dna repair , proliferating cell nuclear antigen , cell cycle checkpoint , microbiology and biotechnology , kinase , suppressor , transcription factor , dna , cell , cancer research , genetics , cancer , gene
The human tumour suppressor protein p53 is critical for regulation of the cell cycle on genotoxic insult. When DNA is damaged by radiation, chemicals or viral infection, cells respond rapidly by arresting the cell cycle. A G 1 arrest requires the activity of wild‐type p53, as it is not observed in cells lacking functionally wild‐type protein, and at least some component of S phase and G 2 /M arrests is also thought to be p53‐dependent. p53 functions as a transcription factor which binds specific DNA sequences, and recently major downstream targets have been identified, including p21 Cip1 an inhibitor of the cell cycle kinases that also blocks the replicative but not the repair function of DNA polymerase δ auxiliary factor, PCNA. Current interest focuses on developing novel cancer therapies based on our knowledge of the activity of p53 and p21 Cip1 in the cell cycle.