The role of NBS1 in the modulation of PIKK family proteins ATM and ATR in the cellular response to DNA damage

Cancer Letters
Junqing ZhouYing Zhang

Abstract

Ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) kinases have been considered the primary activators of the cellular response to DNA damage. They belong to the protein kinase family, phosphoinositide 3-kinase-related kinase (PIKKs). In human beings, deficiency of these kinases leads to hereditary diseases, namely ataxia telangiectasia (AT) with ATM deficiency and ATR-Seckel with ATR deficiency. NBS1, a component of MRE11/RAD50/NBS1 (MRN) complex, is another important player in DNA damage response (DDR). Mutations of NBS1 are responsible for Nijmegen breakage syndrome (NBS), a human hereditary disease with the characteristics that almost encompassed those of AT and ATR-Seckel. NBS1 has been conventionally thought to be a downstream substrate of ATM and ATR in DDR; however, recent studies suggest that NBS1/MRN functions upstream of both ATM and ATR by recruiting them to the proximity of DNA damage sites and activating their functions. In this mini-review, we would emphasize the requirement of NBS1 as an upstream mediator for the modulation of PIKK family proteins ATM and ATR.

References

Dec 15, 1992·Proceedings of the National Academy of Sciences of the United States of America·A DvirW S Dynan
Aug 21, 1992·Cell·B Vogelstein, K W Kinzler
Sep 1, 1995·Genomics·J H PetriniD T Weaver
Apr 2, 1996·Proceedings of the National Academy of Sciences of the United States of America·K A CimprichS L Schreiber
Nov 27, 2001·Science·D CortezS J Elledge
May 4, 2002·Nature Reviews. Molecular Cell Biology·Damien D'Amours, Stephen P Jackson
May 23, 2002·Carcinogenesis·Stephen P Jackson
Oct 26, 2002·Proceedings of the National Academy of Sciences of the United States of America·Hui ZhaoHelen Piwnica-Worms
Nov 26, 2002·Trends in Cell Biology·Alexander J OsbornLee Zou
Jan 30, 2003·Cell·Jason Perry, Nancy Kleckner
Mar 26, 2003·Cell·Stephan GruberKim Nasmyth
Apr 16, 2003·Cell Cycle·Yosef Shiloh
Jun 7, 2003·Science·Lee Zou, Stephen J Elledge
Oct 9, 2003·The EMBO Journal·Tamar UzielYosef Shiloh
Dec 6, 2003·The EMBO Journal·Christian T CarsonMatthew D Weitzman
Jan 1, 2004·Molecular and Cellular Biology·Junran ZhangFen Xia
Jan 20, 2004·Molecular and Cellular Biology·Keziban Unsal-Kaçmaz, Aziz Sancar
Jul 29, 2004·DNA Repair·Ebba U Kurz, Susan P Lees-Miller
Sep 24, 2004·DNA Repair·Eric Weterings, Dik C van Gent
Dec 14, 2004·Oncogene·Spencer J CollisAntony R Parker
Dec 24, 2004·The EMBO Journal·Tom StiffPenny A Jeggo
Feb 3, 2005·Environmental and Molecular Mutagenesis·Masamitsu Honma
Apr 12, 2005·Nature Medicine·Pierre-Olivier FrappartZhao-Qi Wang

❮ Previous
Next ❯

Citations

Jul 21, 2007·Nature Immunology·Mila JankovicMichel C Nussenzweig
Jan 22, 2008·Antioxidants & Redox Signaling·Fabio AltieriSilvia Chichiarelli
Jul 25, 2012·Molecular and Cellular Biology·Kate BeishlineJane Azizkhan-Clifford
Sep 24, 2010·Cell Communication and Signaling : CCS·Alyson K Freeman, Alvaro Na Monteiro
Apr 13, 2012·Breast Cancer Research : BCR·Ying YanKenneth H Cowan
Aug 3, 2013·Antioxidants & Redox Signaling·Bruce C McKay
Jan 25, 2008·Trends in Cell Biology·Myriam Gorospe, Rafael de Cabo
Feb 23, 2008·Current Biology : CB·Małgorzata OklejewiczGijsbertus T J van der Horst
Aug 25, 2007·The Journal of Biological Chemistry·Jie Jessie Lin, Anindya Dutta
Feb 3, 2007·The Journal of Biological Chemistry·Nozomi TomimatsuAkihiro Kurimasa
Jan 1, 2012·Lung Cancer International·Naoko OkumuraSatoru Matsuda

❮ Previous
Next ❯

Related Concepts

Related Feeds

Ataxia telangiectasia

Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.

Ataxia telangiectasia (MDS)

Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.