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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Ataxia telangiectasia mutated

Ataxia telangiectasia mutated
Top mentioned proteins: Atm, p53, H2A, Histone, Chk2
Papers on Ataxia telangiectasia mutated
ATM-dependent Phosphorylation of the Fanconi Anemia Protein PALB2 Promotes the DNA Damage Response.
Huen et al., Hong Kong, Hong Kong. In J Biol Chem, Dec 2015
IR treatment specifically triggered PALB2 phosphorylation at Ser-157 and Ser-376 in manners that required the master DNA damage response kinase Ataxia telangiectasia mutated, revealing potential mechanistic links between PALB2 and the Ataxia telangiectasia mutated-dependent DNA damage responses.
Ataxia Telangiectasia Mutated (ATM) Dysregulation Results in Diabetic Retinopathy.
Grant et al., East Lansing, United States. In Stem Cells, Nov 2015
UNASSIGNED: Ataxia telangiectasia mutated (ATM) acts as a defense against a variety of bone marrow (BM) stressors.
Hyperoxia activates ATM independent from mitochondrial ROS and dysfunction.
O'Reilly et al., Rochester, United States. In Redox Biol, Aug 2015
Ataxia telangiectasia mutated (ATM) kinase is activated by nuclear DNA double strand breaks and delays hyperoxia-induced cell death through downstream targets p53 and p21.
Mechanistic Rationale to Target PTEN-Deficient Tumor Cells with Inhibitors of the DNA Damage Response Kinase ATM.
Kennedy et al., Belfast, United Kingdom. In Cancer Res, Jul 2015
Ataxia telangiectasia mutated (ATM) is an important signaling molecule in the DNA damage response (DDR).
Aberrant TCRδ rearrangement underlies the T-cell lymphocytopenia and t(12;14) translocation associated with ATM deficiency.
Zha et al., Boston, United States. In Blood, May 2015
Ataxia telangiectasia mutated (ATM) is a protein kinase and a master regulator of DNA-damage responses.
ATM has a major role in the double-strand break repair pathway dysregulation in sporadic breast carcinomas and is an independent prognostic marker at both mRNA and protein levels.
Bièche et al., Paris, France. In Br J Cancer, Apr 2015
BACKGROUND: Ataxia telangiectasia mutated (ATM) is a kinase that has a central role in the maintenance of genomic integrity by activating cell cycle checkpoints and promoting repair of DNA double-strand breaks (DSB).
Agrobacterium T-DNA integration into the plant genome can occur without the activity of key non-homologous end-joining proteins.
Gelvin et al., West Lafayette, United States. In Plant J, Mar 2015
In animal cells, several proteins, including KU70, KU80, ARTEMIS, DNA-PKcs, DNA ligase IV (LIG4), Ataxia telangiectasia mutated (ATM), and ATM- and Rad3-related (ATR), play an important role in 'classical' (c)NHEJ.
Tyrosine 370 phosphorylation of ATM positively regulates DNA damage response.
Hung et al., Houston, United States. In Cell Res, Feb 2015
Ataxia telangiectasia mutated (ATM) mediates DNA damage response by controling irradiation-induced foci formation, cell cycle checkpoint, and apoptosis.
The stress-responsive gene ATF3 regulates the histone acetyltransferase Tip60.
Yan et al., Augusta, United States. In Nat Commun, 2014
Tat-interactive protein 60 (Tip60) is a MYST histone acetyltransferase that catalyses acetylation of the major DNA damage kinase Ataxia telangiectasia mutated (ATM), thereby triggering cellular signalling required for the maintenance of genomic stability on genotoxic insults.
XCIND as a genetic disease of X-irradiation hypersensitivity and cancer susceptibility.
Takagi et al., Tokyo, Japan. In Int J Hematol, 2013
Ataxia telangiectasia (A-T) is one such disease, and is caused by biallelic germline mutation of the Ataxia telangiectasia mutated (ATM) gene.
Analysis of individual molecular events of DNA damage response by flow- and image-assisted cytometry.
Wlodkowic et al., Valhalla, United States. In Methods Cell Biol, 2010
Examples of cytometric detection of activation of Ataxia telangiectasia mutated (ATM), and Check 2 (Chk2) protein kinases using phospho-specific Abs targeting Ser1981 and Thr68 of these proteins, respectively are also presented.
Spatiotemporal characterization of ionizing radiation induced DNA damage foci and their relation to chromatin organization.
Jakob et al., Berkeley, United States. In Mutat Res, 2010
Discussion is limited to RIF formed by three interrelated proteins ATM (Ataxia telangiectasia mutated), 53BP1 (p53 binding protein 1) and gammaH2AX (phosphorylated variant histone H2AX), with an emphasis on the later.
Single-stranded DNA-binding protein hSSB1 is critical for genomic stability.
Khanna et al., Brisbane, Australia. In Nature, 2008
Ataxia telangiectasia mutated (ATM) kinase phosphorylates hSSB1 in response to DNA double-strand breaks (DSBs).
Cytometry of ATM activation and histone H2AX phosphorylation to estimate extent of DNA damage induced by exogenous agents.
Darzynkiewicz et al., Valhalla, United States. In Cytometry A, 2007
This review covers the topic of cytometric assessment of activation of Ataxia telangiectasia mutated (ATM) protein kinase and histone H2AX phosphorylation on Ser139 in response to DNA damage, particularly the damage that involves formation of DNA double-strand breaks.
The role of NBS1 in the modulation of PIKK family proteins ATM and ATR in the cellular response to DNA damage.
Zhang et al., Fort Collins, United States. In Cancer Lett, 2006
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.
Molecular cloning and functional characterization of zebrafish ATM.
Kishi et al., Boston, United States. In Int J Biochem Cell Biol, 2005
Characterization of ataxia telangiectasia protein.
Molecular cloning and characterization of the catalytic domain of zebrafish homologue of the ataxia-telangiectasia mutated gene.
Xu et al., New Orleans, United States. In Mol Cancer Res, 2004
molecular cloning of the coding sequence of the catalytic domain of the zebrafish homologue of ATM
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