Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination - Wikidata - wikimedia - TriplyDB

Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination

Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination

http://www.wikidata.org/entity/Q37659903

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IgH chain class switch recombination: mechanism and regulation Consecutive interactions with HSP90 and eEF1A underlie a functional maturation and storage pathway of AID in the cytoplasm.Identification of DNA cleavage- and recombination-specific hnRNP cofactors for activation-induced cytidine deaminase Individual substitution mutations in the AID C terminus that ablate IgH class switch recombination.Cell Cycle Regulates Nuclear Stability of AID and Determines the Cellular Response to AID.Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.Functional requirements of AID's higher order structures and their interaction with RNA-binding proteins The SAGA Deubiquitination Module Promotes DNA Repair and Class Switch Recombination through ATM and DNAPK-Mediated γH2AX Formation.UNG protects B cells from AID-induced telomere loss.Decreased somatic hypermutation induces an impaired peripheral B cell tolerance checkpoint.RNA Exosome and Non-coding RNA-Coupled Mechanisms in AID-Mediated Genomic Alterations.Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites.Increased serum IgM, immunodeficiency, and autoimmunity: A clinical series.AID Biology: A pathological and clinical perspective.Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.Depletion of recombination-specific cofactors by the C-terminal mutant of the activation-induced cytidine deaminase causes the dominant negative effect on class switch recombination.Main steps in DNA double-strand break repair: an introduction to homologous recombination and related processes.A licensing step links AID to transcription elongation for mutagenesis in B cells.Transient AID expression for in situ mutagenesis with improved cellular fitness.AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice

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Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination

http://www.wikidata.org/entity/Q37659903

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 03 March 2014

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Activation induced deaminase C ...... ing class switch recombination

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Activation induced deaminase C ...... ng class switch recombination.

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type

label

Activation induced deaminase C ...... ing class switch recombination

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Activation induced deaminase C ...... ng class switch recombination.

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prefLabel

Activation induced deaminase C ...... ing class switch recombination

@en

Activation induced deaminase C ...... ng class switch recombination.

@nl

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PNAS.1320486111

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

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Activation induced deaminase C ...... ing class switch recombination

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Anil K Eranki

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Anne-Marie Patenaude

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Astrid Zahn

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Elena M Cortizas

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Heather Fifield

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Kohsuke Imai

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Mani Larijani

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Paul Foster

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

Ramiro E Verdun

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P2860

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

Human CtIP promotes DNA end resection

Activation-induced cytidine deaminase initiates immunoglobulin gene conversion and hypermutation by a common intermediate

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

Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis

AID is required to initiate Nbs1/gamma-H2AX focus formation and mutations at sites of class switching

Mismatch recognition and uracil excision provide complementary paths to both Ig switching and the A/T-focused phase of somatic mutation

53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination.

Clinical, immunologic and genetic analysis of 29 patients with autosomal recessive hyper-IgM syndrome due to Activation-Induced Cytidine Deaminase deficiency.

Alternative end-joining catalyzes class switch recombination in the absence of both Ku70 and DNA ligase 4.

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E988-97

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scholarly article

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10.1073/PNAS.1320486111

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11

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111

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Javier M Di Noia

Stephen P Methot

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2014-03-03T00:00:00Z

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260486621

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