Nuclear ataxia-telangiectasia mutated (ATM) mediates the cellular response to DNA double strand breaks in human neuron-like cells
about
Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replicationATM-mediated phosphorylation of polynucleotide kinase/phosphatase is required for effective DNA double-strand break repairATM activates the pentose phosphate pathway promoting anti-oxidant defence and DNA repairATM, the Mre11/Rad50/Nbs1 complex, and topoisomerase I are concentrated in the nucleus of Purkinje neurons in the juvenile human brainAtaxia telangiectasia: a reviewSystematic E2 screening reveals a UBE2D-RNF138-CtIP axis promoting DNA repairATM deficiency results in accumulation of DNA-topoisomerase I covalent intermediates in neural cellsEZH2-mediated H3K27 trimethylation mediates neurodegeneration in ataxia-telangiectasia.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.ATM kinase sustains breast cancer stem-like cells by promoting ATG4C expression and autophagy.USP28 is recruited to sites of DNA damage by the tandem BRCT domains of 53BP1 but plays a minor role in double-strand break metabolism.Inhibition of ataxia telangiectasia mutated kinase activity enhances TRAIL-mediated apoptosis in human melanoma cellsATM-depletion in breast cancer cells confers sensitivity to PARP inhibition.ATM and the epigenetics of the neuronal genome.ATM regulates a DNA damage response posttranscriptional RNA operon in lymphocytesAn essential function for the ATR-activation-domain (AAD) of TopBP1 in mouse development and cellular senescence.Differential roles of ATM- and Chk2-mediated phosphorylations of Hdmx in response to DNA damage.Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?Reactive Oxygen Species (ROS)-Activated ATM-Dependent Phosphorylation of Cytoplasmic Substrates Identified by Large-Scale Phosphoproteomics ScreenWRN is required for ATM activation and the S-phase checkpoint in response to interstrand cross-link-induced DNA double-strand breaks.DNA double-strand break formation upon UV-induced replication stress activates ATM and DNA-PKcs kinases.ATM kinase activity modulates ITCH E3-ubiquitin ligase activity.ATM-dependent phosphorylation of MEF2D promotes neuronal survival after DNA damage.DNA-PKcs is required to maintain stability of Chk1 and Claspin for optimal replication stress responseATM protein kinase: the linchpin of cellular defenses to stress.Brain and induced pluripotent stem cell-derived neural stem cells as an in vitro model of neurodegeneration in ataxia-telangiectasia.ATM-deficient human neural stem cells as an in vitro model system to study neurodegeneration.ATM kinase sustains HER2 tumorigenicity in breast cancer.ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage.Functional switching of ATM: sensor of DNA damage in proliferating cells and mediator of Akt survival signal in post-mitotic human neuron-like cells.Activation of the kinase activity of ATM by retinoic acid is required for CREB-dependent differentiation of neuroblastoma cells.ATM, THMS, and RRM1 protein expression in nasopharyngeal carcinomas treated with curative intent.The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress.A decrease in cyclin B1 levels leads to polyploidization in DNA damage-induced senescence.ATM localization and gene expression in the adult mouse eye.Ataxia telangiectasia mutated (ATM) is essential for DNA-PKcs phosphorylations at the Thr-2609 cluster upon DNA double strand break.Inhibition of poly(ADP-ribose) polymerase (PARP) and ataxia telangiectasia mutated (ATM) on the chemosensitivity of mantle cell lymphoma to agents that induce DNA strand breaks.Matrin-3 is essential for fibroblast growth factor 2-dependent maintenance of neural stem cells
P2860
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P2860
Nuclear ataxia-telangiectasia mutated (ATM) mediates the cellular response to DNA double strand breaks in human neuron-like cells
description
2006 nî lūn-bûn
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2006 թուականի Յունիսին հրատարակուած գիտական յօդուած
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2006 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2006年の論文
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2006年論文
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2006年論文
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2006年論文
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2006年論文
@zh-mo
2006年論文
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2006年论文
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name
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@ast
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@en
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@nl
type
label
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@ast
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@en
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@nl
prefLabel
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@ast
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@en
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@nl
P2093
P2860
P356
P1476
Nuclear ataxia-telangiectasia ...... aks in human neuron-like cells
@en
P2093
Ari Barzilai
Leonid Mittelman
Sharon Biton
Yaron Pereg
Yosef Shiloh
P2860
P304
P356
10.1074/JBC.M601895200
P407
P577
2006-06-23T00:00:00Z