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Immunoglobulin class switch recombination is impaired in Atm-deficient mice

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

http://www.wikidata.org/entity/Q24647660

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ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks Essential role for DNA-PKcs in DNA double-strand break repair and apoptosis in ATM-deficient lymphocytes Lack of MSH2 involvement differentiates V(D)J recombination from other non-homologous end joining events Ataxia-telangiectasia: future prospects IgH chain class switch recombination: mechanism and regulation Ataxia telangiectasia: a review ATM limits incorrect end utilization during non-homologous end joining of multiple chromosome breaks A rat model of ataxia-telangiectasia: evidence for a neurodegenerative phenotype.Regulation of pairing between broken DNA-containing chromatin regions by Ku80, DNA-PKcs, ATM, and 53BP1 A regulatory role for NBS1 in strand-specific mutagenesis during somatic hypermutation Multiple autophosphorylation sites are dispensable for murine ATM activation in vivo Critical role for mouse marginal zone B cells in PF4/heparin antibody production.Role of the translocation partner in protection against AID-dependent chromosomal translocations Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation.ATM increases activation-induced cytidine deaminase activity at downstream S regions during class-switch recombination.53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombination.Genomic instability, endoreduplication, and diminished Ig class-switch recombination in B cells lacking Nbs1.Artemis-independent functions of DNA-dependent protein kinase in Ig heavy chain class switch recombination and development Different mutation signatures in DNA polymerase eta- and MSH6-deficient mice suggest separate roles in antibody diversification Genomic instability, defective spermatogenesis, immunodeficiency, and cancer in a mouse model of the RIDDLE syndrome Regulation of immunoglobulin class-switch recombination: choreography of noncoding transcription, targeted DNA deamination, and long-range DNA repair.The ATM cofactor ATMIN protects against oxidative stress and accumulation of DNA damage in the aging brain.DNA double-strand break signaling and human disorders.Loss of ATM kinase activity leads to embryonic lethality in mice A precocious cerebellar ataxia and frequent Fever episodes in a 16-month-old infant revealing ataxia-telangiectasia syndrome.Role of Nbs1 in the activation of the Atm kinase revealed in humanized mouse models.ATM activation in the presence of oxidative stress.Mechanism and regulation of class switch recombination Ten new ATM alterations in Polish patients with ataxia-telangiectasia.Epigenetic tethering of AID to the donor switch region during immunoglobulin class switch recombination.Altered mucosal immune response after acute lung injury in a murine model of Ataxia Telangiectasia.DNA repair mechanisms in cancer development and therapy p53 represses class switch recombination to IgG2a through its antioxidant function The E3 ubiquitin ligase Mule acts through the ATM-p53 axis to maintain B lymphocyte homeostasis.ATM deficiency impairs thymocyte maturation because of defective resolution of T cell receptor alpha locus coding end breaks.B Cell-Intrinsic Expression of the HuR RNA-Binding Protein Is Required for the T Cell-Dependent Immune Response In Vivo.Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice Role of genomic instability and p53 in AID-induced c-myc-Igh translocations.Activation-induced cytidine deaminase-initiated off-target DNA breaks are detected and resolved during S phase.DNA lesions and repair in immunoglobulin class switch recombination and somatic hypermutation.

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P2860

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

http://www.wikidata.org/entity/Q24647660

description

2004 nî lūn-bûn

@nan

2004 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2004 թվականի նոյեմբերին հրատարակված գիտական հոդված

@hy

2004年の論文

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2004年論文

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2004年論文

@zh-hant

2004年論文

@zh-hk

2004年論文

@zh-mo

2004年論文

@zh-tw

2004年论文

@wuu

name

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@ast

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@en

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@nl

type

label

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@ast

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@en

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@nl

prefLabel

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@ast

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@en

Immunoglobulin class switch recombination is impaired in Atm-deficient mice

@nl

P1433

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Journal of Experimental Medicine

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Immunoglobulin class switch recombination is impaired in Atm-deficient mice

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Carrolee Barlow

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Edward E Max

http://www.w3.org/2001/XMLSchema#string

Joanne M Lumsden

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Lisa K Petiniot

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Patricia J Gearhart

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Rhuna Shen

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Thomas A Wynn

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Thomas McCarty

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P2860

ATM phosphorylates p95/nbs1 in an S-phase checkpoint pathway

ATM-dependent phosphorylation of nibrin in response to radiation exposure

Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2)

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

The many substrates and functions of ATM

DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation

Ataxia telangiectasia mutated (ATM) kinase and ATM and Rad3 related kinase mediate phosphorylation of Brca1 at distinct and overlapping sites. In vivo assessment using phospho-specific antibodies

AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification

Checking in on Cds1 (Chk2): A checkpoint kinase and tumor suppressor

53BP1 and NFBD1/MDC1-Nbs1 function in parallel interacting pathways activating ataxia-telangiectasia mutated (ATM) in response to DNA damage

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1111-21

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scholarly article

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1323087

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10.1084/JEM.20041074

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9

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200

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Anthony Wynshaw-Boris

Herbert C. Morse

Richard J. Hodes

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2004-11-01T00:00:00Z

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8212053

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15504820

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2211853

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