Activation-induced cytidine deaminase targets DNA at sites of RNA polymerase II stalling by interaction with Spt5 - Wikidata - awgldk - TriplyDB

Activation-induced cytidine deaminase targets DNA at sites of RNA polymerase II stalling by interaction with Spt5

Activation-induced cytidine deaminase targets DNA at sites of RNA polymerase II stalling by interaction with Spt5

http://www.wikidata.org/entity/Q34357060

about

Genome instability and transcription elongation impairment in human cells depleted of THO/TREX Histone chaperone Spt6 is required for class switch recombination but not somatic hypermutation Solubility-based genetic screen identifies RING finger protein 126 as an E3 ligase for activation-induced cytidine deaminase 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 Epigenetics of Peripheral B-Cell Differentiation and the Antibody Response Leukemogenic rearrangements at the mixed lineage leukemia gene (MLL)-multiple rather than a single mechanism Regulation of Aicda expression and AID activity Transcriptional stalling in B-lymphocytes: a mechanism for antibody diversification and maintenance of genomic integrity The Spt4-Spt5 complex: a multi-faceted regulator of transcription elongation Related Mechanisms of Antibody Somatic Hypermutation and Class Switch Recombination IgH chain class switch recombination: mechanism and regulation Activation-induced deoxycytidine deaminase (AID) co-transcriptional scanning at single-molecule resolution.Architecture of the RNA polymerase-Spt4/5 complex and basis of universal transcription processivity A functional interface at the rDNA connects rRNA synthesis, pre-rRNA processing and nucleolar surveillance in budding yeast Ubiquitous transcription factors display structural plasticity and diverse functions: NusG proteins - Shifting shapes and paradigms AID/APOBEC deaminases and cancer RNA Exosome Regulates AID DNA Mutator Activity in the B Cell Genome Convergent transcription at intragenic super-enhancers targets AID-initiated genomic instability AID targeting: old mysteries and new challenges APOBEC3A and APOBEC3B Preferentially Deaminate the Lagging Strand Template during DNA Replication The splicing regulator PTBP2 interacts with the cytidine deaminase AID and promotes binding of AID to switch-region DNA Simultaneous in vitro characterisation of DNA deaminase function and associated DNA repair pathways ATAD5 deficiency decreases B cell division and Igh recombination Rif1 prevents resection of DNA breaks and promotes immunoglobulin class switching Analysis of a single-stranded DNA-scanning process in which activation-induced deoxycytidine deaminase (AID) deaminates C to U haphazardly and inefficiently to ensure mutational diversity AID and Apobec3G haphazard deamination and mutational diversity Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2.AID-induced remodeling of immunoglobulin genes and B cell fate.A meiosis-specific Spt5 homolog involved in non-coding transcription.Eμ and 3'RR IgH enhancers show hierarchic unilateral dependence in mature B-cells.Generation and repair of AID-initiated DNA lesions in B lymphocytes.Whole-genome reconstruction and mutational signatures in gastric cancer.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.AID induces double-strand breaks at immunoglobulin switch regions and c-MYC causing chromosomal translocations in yeast THO mutants.Classical Mus musculus Igκ enhancers support transcription but not high level somatic hypermutation from a V-lambda promoter in chicken DT40 cells.High resolution analysis of the chromatin landscape of the IgE switch region in human B cells RNA polymerase II transcription elongation and Pol II CTD Ser2 phosphorylation: A tail of two kinases.Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness

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Activation-induced cytidine deaminase targets DNA at sites of RNA polymerase II stalling by interaction with Spt5

http://www.wikidata.org/entity/Q34357060

description

2010 nî lūn-bûn

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2010 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Activation-induced cytidine de ...... lling by interaction with Spt5

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J.CELL.2010.09.017

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Camilo Ansarah-Sobrinho

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David E Root

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Isaac Klein

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Michela Di Virgilio

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Mila Jankovic

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Rafael Casellas

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Rushad Pavri

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Thomas J Nieland

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Vasco Barreto

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Wolfgang Resch

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P2860

Structure and function of the human transcription elongation factor DSIF

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

DSIF, a novel transcription elongation factor that regulates RNA polymerase II processivity, is composed of human Spt4 and Spt5 homologs

Interaction between antibody-diversification enzyme AID and spliceosome-associated factor CTNNBL1

TIF1gamma controls erythroid cell fate by regulating transcription elongation

Transcriptional analysis of the B cell germinal center reaction

Transcription elongation factor hSPT5 stimulates mRNA capping

Reprogramming towards pluripotency requires AID-dependent DNA demethylation

c-Myc regulates transcriptional pause release

RNA polymerase stalling at developmental control genes in the Drosophila melanogaster embryo

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122-133

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Michel C. Nussenzweig

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47298450

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2993080

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