Evidence map›Paper›PMID 18541713›Full record

ArticleThe Journal of experimental medicine2008

Sgamma3 switch sequences function in place of endogenous Sgamma1 to mediate antibody class switching.

Ali A Zarrin, Peter H Goff, Kate Senger, Frederick W Alt

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. BRCT-domain protein BRIT1 influences class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  3. Review
  4. Article
  5. Review
  6. Impaired B cell development and function in the absence of IkappaBNS.Journal of immunology (Baltimore, Md. : 1950) · 2011
    Article
  7. Overlapping activation-induced cytidine deaminase hotspot motifs in Ig class-switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  8. Article
  9. 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

4 authors at 2 institutions in 1 country.

Ali A ZarrinDepartment of Genetics, Howard Hughes Medical Institute, Children's Hospital, Immune Disease Institute, Harvard University Medical School, Boston, MA 02115, USA.
Peter H Goff
Kate Senger
Frederick W Alt
Harvard University · USHoward Hughes Medical Institute · US

Funding

Transcriptional Regulation of the Allergic ResponseP01AI031541 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 1999 to 2007
$8.0M
MOLECULAR BASIS OF IMMUNE FUNCTION IN HEALTH AND DISEASEU01AI031541 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 1991 to 1994
–
MOLECULAR BASIS OF IMMUNE FUNCTION IN HEALTH AND DISEASEU19AI031541 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 1995 to 1998
–
Howard Hughes Medical InstituteNIAID NIH HHS AI31541NIAID NIH HHS P01 AI031541NIAID NIH HHS U19 AI031541
6 · The paper itself

Abstract

Immunoglobulin heavy chain (IgH) class switch recombination (CSR) replaces the initially expressed IgH Cmu exons with a set of downstream IgH constant region (C(H)) exons. Individual sets of C(H) exons are flanked upstream by long (1-10-kb) repetitive switch (S) regions, with CSR involving a deletional recombination event between the donor Smu region and a downstream S region. Targeting CSR to specific S regions might be mediated by S region-specific factors. To test the role of endogenous S region sequences in targeting specific CSR events, we generated mutant B cells in which the endogenous 10-kb Sgamma1 region was replaced with wild-type (WT) or synthetic 2-kb Sgamma3 sequences or a synthetic 2-kb Sgamma1 sequence. We found that both the inserted endogenous and synthetic Sgamma3 sequences functioned similarly to a size-matched synthetic Sgamma1 sequence to mediate substantial CSR to IgG1 in mutant B cells activated under conditions that stimulate IgG1 switching in WT B cells. We conclude that Sgamma3 can function similarly to Sgamma1 in mediating endogenous CSR to IgG1. The approach that we have developed will facilitate assays for IgH isotype-specific functions of other endogenous S regions.

Indexed as

MutationRecombination, GeneticAnimalsB-LymphocytesGene Rearrangement, B-Lymphocyte, Heavy ChainImmunoglobulin Constant RegionsImmunoglobulin Heavy ChainsMiceMice, TransgenicImmunoglobulin Constant RegionsImmunoglobulin Heavy Chains

Identifiers

PMID18541713
PMCPMC2442634
OpenAlexW2082778626

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.