IMR Press / FBL / Volume 13 / Issue 1 / DOI: 10.2741/2674

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Loss of p53-regulatory protein IFI16 induces NBS1 leading to activation of p53-mediated checkpoint by phosphorylation of p53 SER37
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1 Department of Oncological Sciences, The Mount Sinai School of Medicine, New York University, New York, NY
2 Robert H. Lurie Comprehensive Cancer Center, Basic Sciences Research Division, Northwestern University, Chicago, IL
3 Systems Genome Biology Program, ENH, Department of Medicine, Feinberg School of Medicine, Northwestern University, Evanston, IL
4 Department of Biological Chemistry, University of California Irvine School of Medicine, Irvine, CA
Front. Biosci. (Landmark Ed) 2008, 13(1), 240–248; https://doi.org/10.2741/2674
Published: 1 January 2008
Abstract

Our previous results that IFI16 is involved in p53 transcription activity under conditions of ionizing radiation (IR), and that the protein is frequently lost in human breast cancer cell lines and breast adenocarcinoma tissues suggesting that IFI16 plays a crucial role in controlling cell growth. Here, we show that loss of IFI16 by RNA interference in cell culture causes elevated phosphorylation of p53 Ser37 and accumulated NBS1 (nibrin) and p21WAF1, leading to growth retardation. Consistent with these observations, doxycyclin-induced NBS1 caused accumulation of p21WAF1 and increased phosphorylation of p53 Ser37, leading to cell cycle arrest in G1 phase. Wortmannin treatment was found to decrease p53 Ser37 phosphorylation in NBS-induced cells. These results suggest that loss of IFI16 activates p53 checkpoint through NBS1-DNA-PKcs pathway.

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