Regulation of class switch recombination and somatic mutation by AID phosphorylation - Wikidata - awgldk - TriplyDB

Regulation of class switch recombination and somatic mutation by AID phosphorylation

Regulation of class switch recombination and somatic mutation by AID phosphorylation

http://www.wikidata.org/entity/Q36946561

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The Eph-receptor A7 is a soluble tumor suppressor for follicular lymphoma The RNA exosome targets the AID cytidine deaminase to both strands of transcribed duplex DNA substrates Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity Transcriptional stalling in B-lymphocytes: a mechanism for antibody diversification and maintenance of genomic integrity Related Mechanisms of Antibody Somatic Hypermutation and Class Switch Recombination IgH chain class switch recombination: mechanism and regulation AID/APOBEC deaminases and cancer The interaction between AID and CIB1 is nonessential for antibody gene diversification by gene conversion or class switch recombination Fine-mapping of IgE-associated loci 1q23, 5q31, and 12q13 using 1000 Genomes Project data.Integrity of the AID serine-38 phosphorylation site is critical for class switch recombination and somatic hypermutation in mice Haploinsufficiency of activation-induced deaminase for antibody diversification and chromosome translocations both in vitro and in vivo.Two forms of activation-induced cytidine deaminase differing in their ability to bind agarose.AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations.A coming-of-age story: activation-induced cytidine deaminase turns 10.Colocalization of somatic and meiotic double strand breaks near the Myc oncogene on mouse chromosome 15.Deep-sequencing identification of the genomic targets of the cytidine deaminase AID and its cofactor RPA in B lymphocytes Binding of AID to DNA does not correlate with mutator activity.Recombinant retroviral production and infection of B cells.Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness Regulation of immunoglobulin class-switch recombination: choreography of noncoding transcription, targeted DNA deamination, and long-range DNA repair.AID and somatic hypermutation.Lysine residue at position 22 of the AID protein regulates its class switch activity.Specific recruitment of protein kinase A to the immunoglobulin locus regulates class-switch recombination.Activation-induced cytidine deaminase targets DNA at sites of RNA polymerase II stalling by interaction with Spt5 Complex regulation and function of activation-induced cytidine deaminase.Ribonomic approaches to study the RNA-binding proteome.Cytoplasmic activation-induced cytidine deaminase (AID) exists in stoichiometric complex with translation elongation factor 1α (eEF1A).Parp3 negatively regulates immunoglobulin class switch recombination.Cell Cycle Regulates Nuclear Stability of AID and Determines the Cellular Response to AID.Plasmodium Infection Promotes Genomic Instability and AID-Dependent B Cell Lymphoma.Activation-induced cytidine deaminase (AID) linking immunity, chronic inflammation, and cancer Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.Combinatorial mechanisms regulating AID-dependent DNA deamination: interacting proteins and post-translational modifications.Regulation of activation-induced cytidine deaminase DNA deamination activity in B-cells by Ser38 phosphorylation.Regulation of AID, the B-cell genome mutator.Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers.Improved methodology for the affinity isolation of human protein complexes expressed at near endogenous levels.PARP activation promotes nuclear AID accumulation in lymphoma cells T cell-dependent IgM memory B cells generated during bacterial infection are required for IgG responses to antigen challenge.AID expression increased by TNF-α is associated with class switch recombination of Igα gene in cancers.

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P2860

Regulation of class switch recombination and somatic mutation by AID phosphorylation

http://www.wikidata.org/entity/Q36946561

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Regulation of class switch recombination and somatic mutation by AID phosphorylation

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type

label

Regulation of class switch recombination and somatic mutation by AID phosphorylation

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prefLabel

Regulation of class switch recombination and somatic mutation by AID phosphorylation

@en

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P1476

Regulation of class switch recombination and somatic mutation by AID phosphorylation

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Brian T Chait

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Eileen M Woo

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Kevin M McBride

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Tanja A Schwickert

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P2860

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

Activation-induced cytidine deaminase shuttles between nucleus and cytoplasm like apolipoprotein B mRNA editing catalytic polypeptide 1

MicroRNA-155 suppresses activation-induced cytidine deaminase-mediated Myc-Igh translocation

MicroRNA-155 is a negative regulator of activation-induced cytidine deaminase

The RAG proteins and V(D)J recombination: complexes, ends, and transposition

Transcription enhances AID-mediated cytidine deamination by exposing single-stranded DNA on the nontemplate strand

Transcription-targeted DNA deamination by the AID antibody diversification enzyme

Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas

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

Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells

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2585-2594

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10.1084/JEM.20081319

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11

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205

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Michel C. Nussenzweig

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23303004

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18838546

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phosphorylation

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2571933

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