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The p53-caspase-2 axis in the cell cycle and DNA damage response

  • 작성자

    Sharad Kumar AM FAA FAHMS
  • 작성일자

    2021-06-17
  • 조회수

    318
Sharad Kumar AM FAA FAHMS ( sharad.kumar@unisa.edu.au )
2020 - current Chair of Cancer Biology & Research Professor of Cell Biology, Centre for Cancer Biology, University of South Australia, Australia Affiliate Professor of Medicine, University of Adelaide, Australia
2009 - 2020 Co-Director Centre for Cancer Biology, Adelaide, Australia Research Professor, University of South Australia, Australia NHMRC Senior Principal Research Fellow, UniSA
2004 - 2009 NHMRC Senior Principal Research Fellow, Hanson Institute, IMVS, Adelaide, Australia Affiliate Professor of Medicine, University of Adelaide, Australia
2001 - 2003 NHMRC Principal Research Fellow, Hanson Institute, IMVS, Adelaide, Australia Affiliate Professor of Medicine, University of Adelaide, Australia
1995 - 2000 Florey Research Fellow (1995), Royal Adelaide Hospital Wellcome Trust Senior Research Fellow (1996-2000), Hanson Centre for Cancer Research, IMVS, Adelaide, Australia
1991 -1994 Associate Member, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan

The p53-caspase-2 axis in the cell cycle and DNA damage response

Caspase-2 was discovered almost three decades ago. It was one of the first two mammalian homologs of CED-3, the other being interleukin 1β-converting enzyme (ICE/caspase-1). Despite high similarity with CED-3 and its fly and mammalian counterparts (DRONC and caspase-9, respectively), the function of caspase-2 in apoptosis has remained enigmatic. A number of recent studies suggest that caspase-2 plays an important role in the regulation of p53 in response to cellular stress and DNA damage to prevent the proliferation and accumulation of damaged or aberrant cells. Here, we review these recent observations and their implications in caspase-2-mediated cellular death, senescence, and tumor suppression.

Exp Mol Med. 2021 Apr;53(4):517-527. doi: 10.1038/s12276-021-00590-2
https://pubmed.ncbi.nlm.nih.gov/33854186/