The MRN complex in double-strand break repair and telomere maintenance

被引：322

作者：

Lamarche, Brandon J. ^{[1
]}

Orazio, Nicole I. ^{[1
,2
]}

Weitzman, Matthew D. ^{[1
]}

机构：

[1] Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA

[2] Univ Calif San Diego, Div Biol, Grad Program, San Diego, CA 92093 USA

来源：

FEBS LETTERS | 2010年 / 584卷 / 17期

基金：

美国国家卫生研究院;

关键词：

MRN complex; DNA damage; DNA repair; DSB; Telomere; DNA-DAMAGE RESPONSE; DEPENDENT PROTEIN-KINASE; TELANGIECTASIA-LIKE DISORDER; CLASS-SWITCH RECOMBINATION; MRE11; COMPLEX; CELL-CYCLE; HOMOLOGOUS RECOMBINATION; SACCHAROMYCES-CEREVISIAE; ATAXIA-TELANGIECTASIA; ATM ACTIVATION;

D O I：

10.1016/j.febslet.2010.07.029

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Genomes are subject to constant threat by damaging agents that generate DNA double-strand breaks (DSBs). The ends of linear chromosomes need to be protected from DNA damage recognition and end-joining, and this is achieved through protein-DNA complexes known as telomeres. The Mre11-Rad50-Nbs1 (MRN) complex plays important roles in detection and signaling of DSBs, as well as the repair pathways of homologous recombination (HR) and non-homologous end-joining (NHEJ). In addition, MRN associates with telomeres and contributes to their maintenance. Here, we provide an overview of MRN functions at DSBs, and examine its roles in telomere maintenance and dysfunction. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：3682 / 3695

页数：14

共 177 条

[1] Genome instability:: a mechanistic view of its causes and consequences [J].

Aguilera, Andres ;

Gomez-Gonzalez, Belen .

NATURE REVIEWS GENETICS, 2008, 9 (03) :204-217

[2]

Antoccia A, 2006, GENOME DYN, V1, P191, DOI 10.1159/000092508

[3] The Mre11 Complex and the Response to Dysfunctional Telomeres [J].

Attwooll, Claire L. ;

Akpinar, Muege ;

Petrini, John H. J. .

MOLECULAR AND CELLULAR BIOLOGY, 2009, 29 (20) :5540-5551

[4] The CDK regulates repair of double-strand breaks by homologous recombination during the cell cycle [J].

Aylon, Y ;

Liefshitz, B ;

Kupiec, M .

EMBO JOURNAL, 2004, 23 (24) :4868-4875

[5] DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation [J].

Bakkenist, CJ ;

Kastan, MB .

NATURE, 2003, 421 (6922) :499-506

[6] Conditional inactivation of the NBS1 gene in the mouse central nervous system leads to neurodegeneration and disorganization of the visual system [J].

Baranes, Koby ;

Raz-Prag, Dorit ;

Nitzan, Anat ;

Galron, Ronit ;

Ashery-Padan, Ruth ;

Rotenstreich, Ygal ;

Assaf, Yaniv ;

Shiloh, Yosef ;

Wang, Zhao-Qi ;

Barzilai, Ari ;

Solomon, Arieh S. .

EXPERIMENTAL NEUROLOGY, 2009, 218 (01) :24-32

[7] Cancer predisposition and hematopoietic failure in Rad50S/S mice [J].

Bender, CF ;

Sikes, ML ;

Sullivan, R ;

Huye, LE ;

Le Beau, MM ;

Roth, DB ;

Mirzoeva, OK ;

Oltz, EM ;

Petrini, JHJ .

GENES & DEVELOPMENT, 2002, 16 (17) :2237-2251

[8] Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair [J].

Berkovich, Elijahu ;

Monnat, Raymond J., Jr. ;

Kastan, Michael B. .

NATURE CELL BIOLOGY, 2007, 9 (06) :683-U137

[9] At Loose Ends: Resecting a Double-Strand Break [J].

Bernstein, Kara A. ;

Rothstein, Rodney .

CELL, 2009, 137 (05) :807-810

[10] The multiple roles of the Mre11 complex for meiotic recombination [J].

Borde, Valerie .

CHROMOSOME RESEARCH, 2007, 15 (05) :551-563

← 1 2 3 4 5 6 7 8 9 10 →