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

Separate domains of AID are required for somatic hypermutation and class-switch recombination.

Nature immunology - 1 Jul 2004

Shinkura Reiko, Ito Satomi, Begum Nasim A, Nagaoka Hitoshi, Muramatsu Masamichi, Kinoshita Kazuo, Sakakibara Yoshimasa, Hijikata Hiroko, Honjo Tasuku

Abstract excerpt

Activation-induced cytidine deaminase (AID) is essential for class-switch recombination (CSR) and somatic hypermutation (SHM). Mutants with changes in the C-terminal region of AID retain SHM but lose CSR activity. Here we describe five mutants with alterations in the N-terminal region of AID that caused selective deficiency in SHM but retained CSR, suggesting that the CSR and SHM activities of AID may dissociate...

Read the complete abstract on PubMed

Topics

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

Share to Active Transport, Cell Nucleus
Share to AICDA (Activation-Induced Cytidine Deaminase)

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Cytidine Deaminase

Share to Immunoglobulin Class Switching

Share to NIH 3T3 Cells

Share to Nuclear Localization Signals

Share to Somatic Hypermutation, Immunoglobulin

Share to Spleen

Source

Identifiers

PMID: 15195091
DOI: 10.1038/ni1086

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Separate domains of AID are required for somatic hypermutation and class-switch recombination.PMID 15195091Read ↗

C-terminal deletion of AID uncouples class switch recombination from somatic hypermutation and gene conversion.Semantic proximity Read ↗

Depletion of recombination-specific cofactors by the C-terminal mutant of the activation-induced cytidine deaminase causes the dominant negative effect on class switch recombination.Semantic proximity Read ↗

Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.Semantic proximity Read ↗

AID Binds Cooperatively with UNG and Msh2-Msh6 to Ig Switch Regions Dependent upon the AID C TerminusSemantic proximity Read ↗

Activation-induced cytidine deaminase: structure-function relationship as based on the study of mutants.Semantic proximity Read ↗

Mini‐review Activation‐induced cytidine deaminase: a dual role in class‐switch recombination and somatic hypermutationSemantic proximity Read ↗

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

Haploinsufficiency of Activation-Induced Deaminase for Antibody Diversification and Chromosome Translocations both In Vitro and In VivoSemantic proximity Read ↗

Immunoglobulin class-switch recombination deficienciesSemantic proximity Read ↗

AID Biology: A pathological and clinical perspectiveSemantic proximity Read ↗

The function of AID in somatic mutation and class switch recombination: upstream or downstream of DNA breaks.Semantic proximity Read ↗

Biological function of activation-induced cytidine deaminase (AID)Semantic proximity Read ↗

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