Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice - Wikidata - awgldk - TriplyDB

Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

http://www.wikidata.org/entity/Q35109704

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Wild-type p53-induced phosphatase 1 dephosphorylates histone variant gamma-H2AX and suppresses DNA double strand break repair Lymphocyte-specific compensation for XLF/cernunnos end-joining functions in V(D)J recombination Ataxia-telangiectasia: future prospects Loss of p53 Ser18 and Atm results in embryonic lethality without cooperation in tumorigenesis An essential function for NBS1 in the prevention of ataxia and cerebellar defects Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development Chemopreventive Metabolites Are Correlated with a Change in Intestinal Microbiota Measured in A-T Mice and Decreased Carcinogenesis 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.Synaptic activity bidirectionally regulates a novel sequence-specific S-Q phosphoproteome in neurons 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.Differential requirement for H2AX and 53BP1 in organismal development and genome maintenance in the absence of poly(ADP)ribosyl polymerase 1.Histone H2AX stabilizes broken DNA strands to suppress chromosome breaks and translocations during V(D)J recombination Defining the ATM-mediated barrier to tumorigenesis in somatic mammary cells following ErbB2 activation Artemis-independent functions of DNA-dependent protein kinase in Ig heavy chain class switch recombination and development Developmental propagation of V(D)J recombination-associated DNA breaks and translocations in mature B cells via dicentric chromosomes.ATM-deficient thymic lymphoma is associated with aberrant tcrd rearrangement and gene amplification.Mechanisms that can promote peripheral B-cell lymphoma in ATM-deficient mice.The ATM protein: the importance of being active.ATM, a central controller of cellular responses to DNA damage.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.Intestinal bacteria modify lymphoma incidence and latency by affecting systemic inflammatory state, oxidative stress, and leukocyte genotoxicity.Effects of antioxidants on cancer prevention and neuromotor performance in Atm deficient mice.Stable brain ATM message and residual kinase-active ATM protein in ataxia-telangiectasia Oxidative stress in ataxia telangiectasia.Experimental antioxidant therapy in ataxia telangiectasia.Mutations in the microtubule-associated protein 1A (Map1a) gene cause Purkinje cell degeneration 53BP1 mediates the fusion of mammalian telomeres rendered dysfunctional by DNA-PKcs loss or inhibition.Absence of Wip1 partially rescues Atm deficiency phenotypes in mice.Aberrant TCRδ rearrangement underlies the T-cell lymphocytopenia and t(12;14) translocation associated with ATM deficiency.Telomeres, stem cells, senescence, and cancer.Fanconi anemia pathway-deficient tumor cells are hypersensitive to inhibition of ataxia telangiectasia mutated.ATM deficiency impairs thymocyte maturation because of defective resolution of T cell receptor alpha locus coding end breaks.SirT1 modulates the estrogen-insulin-like growth factor-1 signaling for postnatal development of mammary gland in mice.The p75 neurotrophin receptor can induce autophagy and death of cerebellar Purkinje neurons.Overlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte development Redundant and nonredundant functions of ATM and H2AX in αβ T-lineage lymphocytes.Orientation-specific joining of AID-initiated DNA breaks promotes antibody class switching.Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice

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P2860

Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

http://www.wikidata.org/entity/Q35109704

description

2000 nî lūn-bûn

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2000 թուականի Մարտին հրատարակուած գիտական յօդուած

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2000 թվականի մարտին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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Proceedings of the National Academy of Sciences of the United States of America

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Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice

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F W Alt

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G A Rathbun

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L Davidson

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P2860

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

The DNA double-strand break repair gene hMRE11 is mutated in individuals with an ataxia-telangiectasia-like disorder

Interaction between ATM protein and c-Abl in response to DNA damage

The complete sequence of the coding region of the ATM gene reveals similarity to cell cycle regulators in different species

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

Tumour predisposition in mice heterozygous for a targeted mutation in Nf1

Enhanced phosphorylation of p53 by ATM in response to DNA damage

Requirement of ATM-dependent phosphorylation of brca1 in the DNA damage response to double-strand breaks

Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

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3336-3341

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10.1073/PNAS.050584897

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