The ATM protein kinase: regulating the cellular response to genotoxic stress, and more

被引:1211
作者
Shiloh, Yosef [1 ]
Ziv, Yael [1 ]
机构
[1] Tel Aviv Univ, Sackler Sch Med, David & Inez Myers Lab Canc Genet, Dept Human Mol Genet & Biochem, IL-69978 Tel Aviv, Israel
基金
以色列科学基金会;
关键词
DOUBLE-STRAND BREAKS; DNA-DAMAGE RESPONSE; ATAXIA-TELANGIECTASIA GENE; NIGRO-STRIATAL NEURONS; NF-KAPPA-B; DEPENDENT PHOSPHORYLATION; IONIZING-RADIATION; HOMOLOGOUS RECOMBINATION; FUNCTIONAL-LINK; ACTIVATES ATM;
D O I
10.1038/nrm3546
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The protein kinase ataxia-telangiectasia mutated (ATM) is best known for its role as an apical activator of the DNA damage response in the face of DNA double-strand breaks (DSBs). Following induction of DSBs, ATM mobilizes one of the most extensive signalling networks that responds to specific stimuli and modifies directly or indirectly a broad range of targets. Although most ATM research has focused on this function, evidence suggests that ATM-mediated phosphorylation has a role in the response to other types of genotoxic stress. Moreover, it has become apparent that ATM is active in other cell signalling pathways involved in maintaining cellular homeostasis.
引用
收藏
页码:197 / 210
页数:14
相关论文
共 205 条
  • [1] ATM-dependent phosphorylation and accumulation of endogenous BLM protein in response to ionizing radiation
    Ababou, M
    Dutertre, S
    Lécluse, Y
    Onclercq, R
    Chatton, B
    Amor-Guéret, M
    [J]. ONCOGENE, 2000, 19 (52) : 5955 - 5963
  • [2] Differential localization of ATM is correlated with activation of distinct downstream signaling pathways
    Alexander, Angela
    Walker, Cheryl L.
    [J]. CELL CYCLE, 2010, 9 (18) : 3685 - 3686
  • [3] ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS
    Alexander, Angela
    Cai, Sheng-Li
    Kim, Jinhee
    Nanez, Adrian
    Sahin, Mustafa
    MacLean, Kirsteen H.
    Inoki, Ken
    Guan, Kun-Liang
    Shen, Jianjun
    Person, Maria D.
    Kusewitt, Donna
    Mills, Gordon B.
    Kastan, Michael B.
    Walker, Cheryl Lyn
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (09) : 4153 - 4158
  • [4] Requirement of protein phosphatase 5 in DNA-damage-induced ATM activation
    Ali, A
    Zhang, J
    Bao, SD
    Liu, I
    Otterness, D
    Dean, NM
    Abraham, RT
    Wang, XF
    [J]. GENES & DEVELOPMENT, 2004, 18 (03) : 249 - 254
  • [5] Intrinsic mitochondrial dysfunction in ATM-deficient lymphoblastoid cells
    Ambrose, Mark
    Goldstine, Jimena V.
    Gatti, Richard A.
    [J]. HUMAN MOLECULAR GENETICS, 2007, 16 (18) : 2154 - 2164
  • [6] Andegeko Y, 2001, J BIOL CHEM, V276, P38224
  • [7] PIDD Death-Domain Phosphorylation by ATM Controls Prodeath versus Prosurvival PIDDosome Signaling
    Ando, Kiyohiro
    Kernan, Jennifer L.
    Liu, Peter H.
    Sanda, Takaomi
    Logette, Emmanuelle
    Tschopp, Jurg
    Look, A. Thomas
    Wang, Jianlong
    Bouchier-Hayes, Lisa
    Sidi, Samuel
    [J]. MOLECULAR CELL, 2012, 47 (05) : 681 - 693
  • [8] DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
    Bakkenist, CJ
    Kastan, MB
    [J]. NATURE, 2003, 421 (6922) : 499 - 506
  • [9] Enhanced phosphorylation of p53 by ATN in response to DNA damage
    Banin, S
    Moyal, L
    Shieh, SY
    Taya, Y
    Anderson, CW
    Chessa, L
    Smorodinsky, NI
    Prives, C
    Reiss, Y
    Shiloh, Y
    Ziv, Y
    [J]. SCIENCE, 1998, 281 (5383) : 1674 - 1677
  • [10] HYPERSENSITIVITY OF ATAXIA TELANGIECTASIA SKIN FIBROBLASTS TO DNA ALKYLATING-AGENTS
    BARFKNECHT, TR
    LITTLE, JB
    [J]. MUTATION RESEARCH, 1982, 94 (02): : 369 - 382