Evidence map›Paper›PMID 10770810›Full record

ArticleThe Journal of experimental medicine2000

Entry of B cell receptor into signaling domains is inhibited in tolerant B cells.

B C Weintraub, J E Jun, A C Bishop, K M Shokat, M L Thomas, C C Goodnow

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In one paragraph

Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017
    Review
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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

6 authors at 3 institutions in 2 countries.

B C WeintraubAustralian Cancer Research Foundation Genetics Laboratory, Medical Genome Centre, John Curtin School of Medical Research, Canberra 2601, Australia.
J E Jun
A C Bishop
K M Shokat
M L Thomas
C C Goodnow
Australian Cancer Research Foundation · AUPrinceton University · USHoward Hughes Medical Institute · US

Funding

SPECIFIC INHIBITOR OF LCK TO PROBE T CELL SIGNALINGR01AI044009 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHOKAT, KEVAN M. · 1998 to 2006
$2.1M
NIAID NIH HHS R01 AI044009NIAID NIH HHS R01AI44009-01
6 · The paper itself

Abstract

Signal transduction through the B cell antigen receptor (BCR) is altered in B cells that express a receptor that recognizes self-antigen. To understand the molecular basis for the change in signaling in autoreactive B cells, a transgenic model was used to isolate a homogeneous population of tolerant B lymphocytes. These cells were compared with a similar population of naive B lymphocytes. We show that the BCR from naive B cells enters a detergent-insoluble domain of the cell within 6 s after antigen binding, before a detectable increase in BCR phosphorylation. This fraction appears to be important for signaling because it is enriched for lyn kinase but lacks CD45 tyrosine phosphatase and because the BCR that moves into this domain becomes more highly phosphorylated. Partitioning of the BCR into this fraction is unaffected by src family kinase inhibition. Tolerant B cells do not efficiently partition the BCR into the detergent-insoluble domain, providing an explanation for their reduced tyrosine kinase activation and calcium flux in response to antigen. These results identify an early, regulated step in antigen receptor signaling and self-tolerance.

Indexed as

Self ToleranceAnimalsAutoimmunityB-LymphocytesChickensMiceMice, TransgenicMuramidasePhosphorylationReceptors, Antigen, B-CellSignal TransductionMuramidaseReceptors, Antigen, B-Cell

Identifiers

PMID10770810
PMCPMC2193133
OpenAlexW2154581565

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.