Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs. - Wikidata - wikimedia - TriplyDB

Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.

Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.

http://www.wikidata.org/entity/Q36439520

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Direct regulation of CREB transcriptional activity by ATM in response to genotoxic stress Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome mice ATM-Dependent Phosphorylation of All Three Members of the MRN Complex: From Sensor to Adaptor Ataxia-telangiectasia: future prospects Pathogenesis of ataxia-telangiectasia: the next generation of ATM functions Nuclear ataxia-telangiectasia mutated (ATM) mediates the cellular response to DNA double strand breaks in human neuron-like cells Evidence of toxicity, oxidative stress, and neuronal insult in autism Ataxia telangiectasia mutated is essential during adult neurogenesis The identification of zebrafish mutants showing alterations in senescence-associated biomarkers Quantitative analysis of gene expression in living adult neural stem cells by gene trapping Oxidative stress-induced DNA damage and cell cycle regulation in B65 dopaminergic cell line Accumulation of DNA damage and reduced levels of nicotine adenine dinucleotide in the brains of Atm-deficient mice The role of the DNA damage response kinase ataxia telangiectasia mutated in neuroprotection Investigation of the functional link between ATM and NBS1 in the DNA damage response in the mouse cerebellum.A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden.Etoposide induces ATM-dependent mitochondrial biogenesis through AMPK activation The E1A-associated p400 protein modulates cell fate decisions by the regulation of ROS homeostasis.ATM and ataxia telangiectasia.DNA damage in Nijmegen Breakage Syndrome cells leads to PARP hyperactivation and increased oxidative stress.Reducing mitochondrial ROS improves disease-related pathology in a mouse model of ataxia-telangiectasia.The ATM cofactor ATMIN protects against oxidative stress and accumulation of DNA damage in the aging brain.Elevated Cu/Zn-SOD exacerbates radiation sensitivity and hematopoietic abnormalities of Atm-deficient mice Reduced synchronization persistence in neural networks derived from atm-deficient mice.ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulation.Effects of antioxidants on cancer prevention and neuromotor performance in Atm deficient mice.Oxidative stress in ataxia telangiectasia.NADPH oxidase 4 is a critical mediator in Ataxia telangiectasia disease.ATM: sounding the double-strand break alarm.Radiological imaging in ataxia telangiectasia: a review.Experimental antioxidant therapy in ataxia telangiectasia.Heme oxygenase-1 and carbon monoxide modulate DNA repair through ataxia-telangiectasia mutated (ATM) protein.Mouse models for induced genetic instability at endogenous loci.Pathways to motor incoordination: the inherited ataxias.All stressed out without ATM kinase ATM facilitates mouse gammaherpesvirus reactivation from myeloid cells during chronic infection.Ataxia-telangiectasia mutated kinase regulates ribonucleotide reductase and mitochondrial homeostasis Male Rat Germ Cells Display Age-Dependent and Cell-Specific Susceptibility in Response to Oxidative Stress Challenges.An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations.The ATM signaling network in development and disease.Clinical implications of the basic defects in Cockayne syndrome and xeroderma pigmentosum and the DNA lesions responsible for cancer, neurodegeneration and aging

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P2860

Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.

http://www.wikidata.org/entity/Q36439520

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Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.

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Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.

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P2860

Linkage of ATM to cell cycle regulation by the Chk2 protein kinase

Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency

Activation of the ATM kinase by ionizing radiation and phosphorylation of p53

A single ataxia telangiectasia gene with a product similar to PI-3 kinase

Noncyclooxygenase oxidative formation of a series of novel prostaglandins: analytical ramifications for measurement of eicosanoids

Targeted disruption of ATM leads to growth retardation, chromosomal fragmentation during meiosis, immune defects, and thymic lymphoma

Enhanced phosphorylation of p53 by ATM in response to DNA damage

ATM: from gene to function

A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans

Atm-deficient mice: a paradigm of ataxia telangiectasia

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