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

Dependence of nucleotide substitutions on Ung2, Msh2, and PCNA-Ub during somatic hypermutation.

The Journal of experimental medicine - 23 Nov 2009

Krijger Peter H L, Langerak Petra, van den Berk Paul C M, Jacobs Heinz

Abstract excerpt

During somatic hypermutation (SHM), B cells introduce mutations into their immunoglobulin genes to generate high affinity antibodies. Current models suggest a separation in the generation of G/C transversions by the Ung2-dependent pathway and the generation of A/T mutations by the Msh2/ubiquitina...

Read the complete abstract on PubMed

Topics

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

Share to Antibody Affinity
Share to B-Lymphocytes
Share to Mice

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Mutant Strains

Share to MutS Homolog 2 Protein

Share to Proliferating Cell Nuclear Antigen

Share to Somatic Hypermutation, Immunoglobulin

Share to Uracil-DNA Glycosidase

Source

Open in PubMed Open full text

Identifiers

PMID: 19901081
DOI: 10.1084/jem.20091707
PMCID: PMC2806606

Genes

PCNA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-19901081-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dependence of nucleotide substitutions on Ung2, Msh2, and PCNA-Ub during somatic hypermutation.PMID 19901081Read ↗

Pms2 and uracil-DNA glycosylases act jointly in the mismatch repair pathway to generate Ig gene mutations at A-T base pairs.Semantic proximity Read ↗

Mutating for Good: DNA Damage Responses During Somatic HypermutationSemantic proximity Read ↗

Molecular mechanisms of antibody somatic hypermutation.Semantic proximity Read ↗

PCNA ubiquitination-independent activation of polymerase η during somatic hypermutation and DNA damage tolerance.Semantic proximity Read ↗

Known components of the immunoglobulin A:T mutational machinery are intact in Burkitt lymphoma cell lines with G:C bias.Semantic proximity Read ↗

Refining the Neuberger model: Uracil processing by activated B cells.Semantic proximity Read ↗

Uracil excision by endogenous SMUG1 glycosylase promotes efficient Ig class switching and impacts on A:T substitutions during somatic mutation.Semantic proximity Read ↗

UNG shapes the specificity of AID-induced somatic hypermutation.Semantic proximity Read ↗

The concerted action of Msh2 and UNG stimulates somatic hypermutation at A . T base pairs.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 ↗

Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting.Semantic proximity Read ↗

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

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