Evidence map›Paper›PMID 11514602›Full record

ArticleThe Journal of experimental medicine2001

Interference with immunoglobulin (Ig)alpha immunoreceptor tyrosine-based activation motif (ITAM) phosphorylation modulates or blocks B cell development, depending on the availability of an Igbeta cytoplasmic tail.

M Kraus, L I Pao, A Reichlin, Y Hu, B Canono, J C Cambier, M C Nussenzweig, K Rajewsky

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
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  4. CtIP-mediated DNA resection is dispensable for IgH class switch recombination by alternative end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2020
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  10. 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

8 authors at 5 institutions in 2 countries.

M KrausInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany. kraus@cbr.med.harvard.edu
L I Pao
A Reichlin
Y Hu
B Canono
J C Cambier
M C Nussenzweig
K Rajewsky
University of Cologne · DERockefeller University · USHoward Hughes Medical Institute · USNational Jewish Health · USUniversity of Colorado Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To determine the function of immunoglobulin (Ig)alpha immunoreceptor tyrosine-based activation motif (ITAM) phosphorylation, we generated mice in which Igalpha ITAM tyrosines were replaced by phenylalanines (Igalpha(FF/FF)). Igalpha(FF/FF) mice had a specific reduction of B1 and marginal zone B cells, whereas B2 cell development appeared to be normal, except that lambda1 light chain usage was increased. The mutants responded less efficiently to T cell-dependent antigens, whereas T cell-independent responses were unaffected. Upon B cell receptor ligation, the cells exhibited heightened calcium flux, weaker Lyn and Syk tyrosine phosphorylation, and phosphorylation of Igalpha non-ITAM tyrosines. Strikingly, when the Igalpha ITAM mutation was combined with a truncation of Igbeta, B cell development was completely blocked at the pro-B cell stage, indicating a crucial role of ITAM phosphorylation in B cell development.

Indexed as

Amino Acid MotifsAmino Acid SubstitutionAnimalsAntigens, CDBase SequenceB-LymphocytesCD79 AntigensCytoplasmDNAMiceMolecular Sequence DataPhenylalaninePhosphorylationReceptors, FcTyrosineAntigens, CDCD79 AntigensCd79b protein, mouseDNAIgA receptorPhenylalanineReceptors, FcTyrosine

Identifiers

PMID11514602
PMCPMC2193498
OpenAlexW2026043938

What OpenQuestion holds

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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.