Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

AID-associated DNA repair pathways regulate malignant transformation in a murine model of BCL6-driven diffuse large B-cell lymphoma.

Blood - 7 Jan 2016

Gu Xiwen, Booth Carmen J, Liu Zongzhi, Strout Matthew P

Abstract excerpt

Somatic hypermutation and class-switch recombination of the immunoglobulin (Ig) genes occur in germinal center (GC) B cells and are initiated through deamination of cytidine to uracil by activation-induced cytidine deaminase (AID). Resulting uracil-guanine mismatches are processed by uracil DNA glycosylase (UNG)-mediated base-excision repair and MSH2-mediated mismatch repair (MMR) to yield mutations and DNA...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to AICDA (Activation-Induced Cytidine Deaminase)
Share to Cytidine Deaminase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Germinal Center

Share to Immunoglobulin Class Switching

Share to Lymphoma, Large B-Cell, Diffuse

Share to Proto-Oncogene Proteins c-bcl-6

Share to Somatic Hypermutation, Immunoglobulin

Share to Uracil-DNA Glycosidase

Source

Open in PubMed Open full text

Identifiers

PMID: 26385350
DOI: 10.1182/blood-2015-02-628164
PMCID: PMC4705602

Genes

MSH2
UNG
BCL6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

AID-associated DNA repair pathways regulate malignant transformation in a murine model of BCL6-driven diffuse large B-cell lymphoma.PMID 26385350Read ↗

Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphomaSemantic proximity Read ↗

Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.Semantic proximity Read ↗

AID expression in B-cell lymphomas causes accumulation of genomic uracil and a distinct AID mutational signature.Semantic proximity Read ↗

MSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sites.Semantic proximity Read ↗

AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations.Semantic proximity Read ↗

Somatic hypermutation mechanisms during lymphomagenesis and transformation.Semantic proximity Read ↗

UNG protects B cells from AID-induced telomere lossSemantic proximity Read ↗

Oncogenic events triggered by AID, the adverse effect of antibody diversificationSemantic proximity Read ↗

The in vivo pattern of AID targeting to immunoglobulin switch regions deduced from mutation spectra in msh2-/- ung-/- mice.Semantic proximity Read ↗

The mismatch repair pathway functions normally at a non-AID target in germinal center B cells.Semantic proximity Read ↗

The off-target effects of AID in carcinogenesisSemantic proximity Read ↗

A broad atlas of somatic hypermutation allows prediction of activation-induced deaminase targets.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.