Evidence map›Paper›PMID 22078222›Full record

ArticleImmunity2011

Monophosphorylation of CD79a and CD79b ITAM motifs initiates a SHIP-1 phosphatase-mediated inhibitory signaling cascade required for B cell anergy.

Shannon K O'Neill, Andrew Getahun, Stephen B Gauld, Kevin T Merrell, Idan Tamir, Mia J Smith, Joseph M Dal Porto, Quan-Zhen Li, John C Cambier

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

95 citing papers in PubMed, 163 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. CARD19, a Novel Regulator of the TAK1/NF-κB Pathway in Self-Reactive B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  18. Review
  19. Article
  20. Article

35 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Shannon K O'NeillIntegrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health, Denver, CO 80206, USA.
Andrew Getahun
Stephen B Gauld
Kevin T Merrell
Idan Tamir
Mia J Smith
Joseph M Dal Porto
Quan-Zhen Li
John C Cambier
National Jewish Health · USUniversity of Colorado Denver · USThe University of Texas Southwestern Medical Center · US

Funding

THE REGULATION OF V ALPHA 7 EXPRESSING T CELLSP01AI022295 · NIAID · NATIONAL JEWISH HEALTH · PI REFAELI, YOSEF · 1985 to 2011
$11.7M
SIGNAL TRANSDUCTION IN B CELL ACTIVATIONR01AG013983 · NIA · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 1996 to 2010
$3.0M
Infectious Agents and B Cell AnergyR01AI077597 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2010 to 2014
$1.9M
NIAID NIH HHS AI022295NIAID NIH HHS AI077597NIAID NIH HHS P01 AI022295NIAID NIH HHS R01 AI077597NIA NIH HHS AG013989NIA NIH HHS R01 AG013983
6 · The paper itself

Abstract

Anergic B cells are characterized by impaired signaling and activation after aggregation of their antigen receptors (BCR). The molecular basis of this impairment is not understood. In studies reported here, Src homology-2 (SH2)-containing inositol 5-phosphatase SHIP-1 and its adaptor Dok-1 were found to be constitutively phosphorylated in anergic B cells, and activation of this inhibitory circuit was dependent on Src-family kinase activity and consequent to biased BCR immunoreceptor tyrosine-based activation motif (ITAM) monophosphorylation. B cell-targeted deletion of SHIP-1 caused severe lupus-like disease. Moreover, absence of SHIP-1 in B cells led to loss of anergy as indicated by restoration of BCR signaling, loss of anergic surface phenotype, and production of autoantibodies. Thus, chronic BCR signals maintain anergy in part via ITAM monophosphorylation-directed activation of an inhibitory signaling circuit involving SHIP-1 and Dok-1.

Indexed as

Signal TransductionAmino Acid MotifsAnimalsAutoimmunityB-LymphocytesCD79 AntigensCell Line, TumorCells, CulturedClonal AnergyDNA-Binding ProteinsGene TargetingInositol Polyphosphate 5-PhosphatasesMiceMice, TransgenicPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoproteinsCD79 AntigensDNA-Binding ProteinsDok1 protein, mouseInositol Polyphosphate 5-PhosphatasesInpp5d protein, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoproteinsPhosphoric Monoester HydrolasesRNA-Binding Proteinssrc-Family KinasesTyrosine

Identifiers

PMID22078222
PMCPMC3232011
OpenAlexW2011444435

What OpenQuestion holds

Textmetadata
LicenceTDM
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.