AID-initiated DNA lesions are differentially processed in distinct B cell populations. - sprookjes - yvandenbroek - TriplyDB

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

http://www.wikidata.org/entity/Q34550504

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Unexpected effects of different genetic backgrounds on identification of genomic rearrangements via whole-genome next generation sequencing.Imbalanced PTEN and PI3K Signaling Impairs Class Switch Recombination.Combined deletion of Xrcc4 and Trp53 in mouse germinal center B cells leads to novel B cell lymphomas with clonal heterogeneity Interplay between Target Sequences and Repair Pathways Determines Distinct Outcomes of AID-Initiated Lesions Efficient AID targeting of switch regions is not sufficient for optimal class switch recombination.Chemotherapy-induced differential cell cycle arrest in B cell lymphomas affects their sensitivity to Wee1 inhibition.

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AID-initiated DNA lesions are differentially processed in distinct B cell populations.

http://www.wikidata.org/entity/Q34550504

description

2014 nî lūn-bûn

@nan

2014 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հոտեմբերին հրատարակված գիտական հոդված

@hy

2014年の論文

@ja

2014年論文

@yue

2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@ast

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@en

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@nl

type

label

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@ast

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@en

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@nl

prefLabel

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@ast

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@en

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@nl

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JIMMUNOL.1401549

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Journal of Immunology

P1476

AID-initiated DNA lesions are differentially processed in distinct B cell populations.

@en

P2093

Erica Hansen

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

Jing H Wang

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Maxwell D Eder

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Mihret T Elos

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Sawanee S Viboolsittiseri

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Sheila Ranganath

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Shunzong Yuan

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Xiaomi Chen

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Zhangguo Chen

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P2860

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

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

Transcriptional analysis of the B cell germinal center reaction

Immunity through DNA deamination

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

Somatic hypermutation and class switch recombination in Msh6(-/-)Ung(-/-) double-knockout mice

Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting

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

Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme

ATM prevents the persistence and propagation of chromosome breaks in lymphocytes.

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5545-5556

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scholarly article

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10.4049/JIMMUNOL.1401549

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11

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193

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2014-10-22T00:00:00Z

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268984861

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25339658

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4239163

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