Involvement of p29 in DNA damage responses and Fanconi anemia pathway

Carcinogenesis. 2009 Oct;30(10):1710-6. doi: 10.1093/carcin/bgp204. Epub 2009 Sep 11.

Abstract

Human p29 is a chromatin-associated protein and the silencing of p29 expression increases cell population in G(1) phase and decreases phosphorylation levels of Chk1 and Chk2 in response to UV treatment. To further characterize the function of p29, U2OS and Fanconi anemia complementation group G (FA-G) cells with constitutive p29 expression have been established. Analyses of these cells identified increased phosphorylation levels of Chk1 and Chk2, which were accompanied by elevated amounts of chromatin-associated Mre11-Rad50-Nbs1 complex and ATR-IP. Monoubiquitination of the FA ID complex was restored in p29 stably expressing FA-G cells. Moreover, lower tumor incidence was observed in mp29 transgenic mice after UV irradiation. These results suggest the involvement of p29 in the DNA damage responses and Fanconi anemia pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Checkpoint Kinase 1
  • Checkpoint Kinase 2
  • Fanconi Anemia / physiopathology*
  • Fanconi Anemia Complementation Group D2 Protein / metabolism
  • HeLa Cells
  • Humans
  • Mice
  • Mice, Transgenic
  • Phosphorylation
  • Protein Kinases / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • RNA, Small Interfering / genetics
  • Ubiquitin / metabolism
  • Ultraviolet Rays

Substances

  • FANCD2 protein, human
  • Fanconi Anemia Complementation Group D2 Protein
  • RNA, Small Interfering
  • Ubiquitin
  • Protein Kinases
  • Checkpoint Kinase 2
  • CHEK1 protein, human
  • CHEK2 protein, human
  • Checkpoint Kinase 1
  • Chek1 protein, mouse
  • Chek2 protein, mouse
  • Protein Serine-Threonine Kinases