PPMID dephosphorylates Chk1 and p53 and abrogates cell cycle checkpoints

Article Abstract:

The oncogenic p53-induced serine/threonine phosphate, PPMID (or Wip1) is found to dephosphorylate two ataxia-telangiectasia mutated (ATM)/ataxia-telangiectasia and Rad3-related (ATR) targets, Chk1 and p53. The primary function of PPMID is to reverse the p53 and Chk1-induced DNA damage and cell cycle checkpoint responses, and return the cell to a homeostatic state following completion of DNA repair.

Gene mutations, Gene mutation, Oncogenes

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Single- and double-stranded DNA: Building a trigger of ATR-mediated DNA damage response

Article Abstract:

The DNA damage signal are generated by the activation of ataxia-telangiectasia mutated and Rad3-related kinase (ATR) checkpoints mediated by single and double stranded DNA fragments formed at the replication forks. These responses produced during DNA replication are known as interference and they distinguish the damaged cells forming an anticancer barrier during early stages of tumor formation.

Ataxia telangiectasia

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p73 induction after DNA damage is regulated by checkpoint kinases Chk1 and Chk2

Article Abstract:

The checkpoint kinases Chk1 and Chk2 are central to the induction of cell cycle arrest, DNA repair, and apoptosis as elements in the DNA-damage checkpoint. Several experimental systems were used to show that interference with or augmentation of Chk1 or Chk2 signaling strongly impacts p73 accumulation and that E2F1 directs p73 expression in the presence and absence of DNA damage.

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