Evidence map›Paper›PMID 18036997›Full record

ArticleDNA repair2008

Brca1 in immunoglobulin gene conversion and somatic hypermutation.

Simonne Longerich, Brian J Orelli, Richard W Martin, Douglas K Bishop, Ursula Storb

Open access · greenAbstract readComparative Study
In one paragraph

Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. SUMOylation of PCNA by PIAS1 and PIAS4 promotes template switch in the chicken and human B cell lines.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  4. Review
  5. Genome complexity in the coelacanth is reflected in its adaptive immune system.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2014
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Temporal regulation of Ig gene diversification revealed by single-cell imaging.Journal of immunology (Baltimore, Md. : 1950) · 2009
    Article
  11. The current structural and functional understanding of APOBEC deaminases.Cellular and molecular life sciences : CMLS · 2009
    Review
  12. Article
  13. Activation-induced cytidine deaminase-mediated hypermutation in the DT40 cell line.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009
    Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Simonne LongerichCommittee on Immunology, University of Chicago, Chicago, IL 60637, USA.
Brian J Orelli
Richard W Martin
Douglas K Bishop
Ursula Storb
University of Chicago · US

Funding

MECHANISM OF IMMUNOGLOBULIN HYPERMUTATIONR01AI047380 · NIAID · UNIVERSITY OF CHICAGO · PI STORB, URSULA B · 2000 to 2010
$4.2M
Immunoglobulin Somatic MutationR01AI053130 · NIAID · UNIVERSITY OF CHICAGO · PI STORB, URSULA B · 2003 to 2007
$1.3M
Mechanism of Immunoglobulin HypermutationR56AI047380 · NIAID · UNIVERSITY OF CHICAGO · PI STORB, URSULA B · 2012 to 2012
$395k
NIAID NIH HHS AI 053130NIAID NIH HHS AI 47380NIAID NIH HHS R01 AI047380NIAID NIH HHS R01 AI053130NIAID NIH HHS R56 AI047380
6 · The paper itself

Abstract

Defects in Brca1 confer susceptibility to breast cancer and genomic instability indicative of aberrant repair of DNA breaks. Brca1 was previously implicated in the homologous recombination pathway via effects on the assembly of recombinase Rad51. Activation-induced cytidine deaminase (AID) deaminates C to U in B lymphocyte immunoglobulin (Ig) DNA to initiate programmed DNA breaks. Subsequent uracil-glycosylase mediated U removal, and perhaps further processing, leads to four known classes of mutation: Ig class switch recombination that results in a region-specific genomic deletion, Ig somatic hypermutation that introduces point mutations in Ig V-regions, Ig gene conversion in vertebrates that possess Ig pseudo-V genes, and translocations common to B cell lymphomas. We tested the involvement of Brca1 in AID-dependent Ig diversification in chicken DT40 cells. The DT40 cell line diversifies IgVlambda mainly by gene conversion, and less so by point mutation. Brca1-deficiency caused a shift in Vlambda diversification, significantly reducing the proportion of gene conversions relative to point mutations. Thus, Brca1 regulates AID-dependent DNA lesion repair. Interestingly, while Brca1 is required to recruit ubiquitinated FancD2 to DNA damage, the phenotype of Brca1-deficient DT40 differs from the one of FancD2-deficient DT40, in which both gene conversion and non-templated mutations are impaired.

Indexed as

DNA RepairAICDA (Activation-Induced Cytidine Deaminase)AnimalsBlotting, SouthernBlotting, WesternB-LymphocytesBRCA1 ProteinCell LineChickensCytidine DeaminaseDNA PrimersFanconi Anemia Complementation Group D2 ProteinGene ConversionHumansImmunoglobulin Variable RegionMutationAICDA (Activation-Induced Cytidine Deaminase)BRCA1 ProteinCytidine DeaminaseDNA PrimersFANCD2 protein, humanFanconi Anemia Complementation Group D2 ProteinImmunoglobulin Variable Region

Identifiers

PMID18036997
PMCPMC2267027
OpenAlexW2093498276

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.