AID expression levels determine the extent of cMyc oncogenic translocations and the incidence of B cell tumor development. - Wikidata - awgldk - TriplyDB

AID expression levels determine the extent of cMyc oncogenic translocations and the incidence of B cell tumor development.

AID expression levels determine the extent of cMyc oncogenic translocations and the incidence of B cell tumor development.

http://www.wikidata.org/entity/Q36853393

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Optimal functional levels of activation-induced deaminase specifically require the Hsp40 DnaJa1 HoxC4 binds to the promoter of the cytidine deaminase AID gene to induce AID expression, class-switch DNA recombination and somatic hypermutation Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity Regulation of Aicda expression and AID activity AID targeting is dependent on RNA polymerase II pausing.ATAD5 deficiency decreases B cell division and Igh recombination Activation-induced cytidine deaminase expression in CD4+ T cells is associated with a unique IL-10-producing subset that increases with age (18)F-FDG-PET/CT imaging in an IL-6- and MYC-driven mouse model of human multiple myeloma affords objective evaluation of plasma cell tumor progression and therapeutic response to the proteasome inhibitor ixazomib.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.IL-6 and MYC collaborate in plasma cell tumor formation in mice.Deep-sequencing identification of the genomic targets of the cytidine deaminase AID and its cofactor RPA in B lymphocytes Origin of chromosomal translocations in lymphoid cancer.B cell TLRs and induction of immunoglobulin class-switch DNA recombination.Agricultural pesticide exposure and the molecular connection to lymphomagenesis.Regulation of microRNA expression and abundance during lymphopoiesis.The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemia.Controlling somatic hypermutation in immunoglobulin variable and switch regions.Msh6 protects mature B cells from lymphoma by preserving genomic stability.AID-targeting and hypermutation of non-immunoglobulin genes does not correlate with proximity to immunoglobulin genes in germinal center B cells.Regulation of activation-induced deaminase stability and antibody gene diversification by Hsp90.Impaired induction of DNA lesions during immunoglobulin class-switch recombination in humans influences end-joining repair.In vivo analysis of Aicda gene regulation: a critical balance between upstream enhancers and intronic silencers governs appropriate expression.B cell super-enhancers and regulatory clusters recruit AID tumorigenic activity.Anaplastic plasmacytoma of mouse--establishing parallels between subtypes of mouse and human plasma cell neoplasia.Lupus-prone MRL/faslpr/lpr mice display increased AID expression and extensive DNA lesions, comprising deletions and insertions, in the immunoglobulin locus: concurrent upregulation of somatic hypermutation and class switch DNA recombination.Translocation of an antibody transgene requires AID and occurs by interchromosomal switching to all switch regions except the mu switch region.Human lymphoid translocation fragile zones are hypomethylated and have accessible chromatin.p53 represses class switch recombination to IgG2a through its antioxidant function Nonimmunoglobulin target loci of activation-induced cytidine deaminase (AID) share unique features with immunoglobulin genes Dendritic cell-mediated activation-induced cytidine deaminase (AID)-dependent induction of genomic instability in human myeloma.Mouse model of endemic Burkitt translocations reveals the long-range boundaries of Ig-mediated oncogene deregulation Anaplastic plasmacytomas: relationships to normal memory B cells and plasma cell neoplasms of immunodeficient and autoimmune mice.Mechanisms of Yin Yang 1 in oncogenesis: the importance of indirect effects.AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway.Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.Regulation of activation-induced cytidine deaminase DNA deamination activity in B-cells by Ser38 phosphorylation.Close proximity to Igh is a contributing factor to AID-mediated translocations.

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AID expression levels determine the extent of cMyc oncogenic translocations and the incidence of B cell tumor development.

http://www.wikidata.org/entity/Q36853393

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2008 nî lūn-bûn

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AID expression levels determin ...... e of B cell tumor development.

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AID expression levels determin ...... e of B cell tumor development.

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AID expression levels determin ...... e of B cell tumor development.

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AID expression levels determin ...... e of B cell tumor development.

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André Nussenzweig

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Elsa Callen

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Frederick W Alt

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Helena Tolarová

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Lionel Feigenbaum

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Makiko Takizawa

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Maria Mosaico

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Michael Potter

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Rafael Casellas

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Sonia Franco

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P2860

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

AID-GFP chimeric protein increases hypermutation of Ig genes with no evidence of nuclear localization.

Internal IgH class switch region deletions are position-independent and enhanced by AID expression

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

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

IgH class switching and translocations use a robust non-classical end-joining pathway

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

Altered somatic hypermutation and reduced class-switch recombination in exonuclease 1-mutant mice

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

Evidence from the generation of immunoglobulin G-secreting cells that stochastic mechanisms regulate lymphocyte differentiation

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10.1084/JEM.20081007

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9

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205

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18678733

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2526190

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