Evidence map›Paper›PMID 7638185›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Restoration of surface IgM-mediated apoptosis in an anti-IgM-resistant variant of WEHI-231 lymphoma cells by HS1, a protein-tyrosine kinase substrate.

T Fukuda, D Kitamura, I Taniuchi, Y Maekawa, L E Benhamou, P Sarthou, T Watanabe

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-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

16 citing papers in PubMed, 63 citations in OpenAlex.

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  11. The B cell-restricted adaptor BASH is required for normal development and antigen receptor-mediated activation of B cells.Proceedings of the National Academy of Sciences of the United States of America · 2000
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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

7 authors at 1 institution in 1 country.

T FukudaDepartment of Molecular Immunology, Kyushu University, Fukuoka, Japan.
D Kitamura
I Taniuchi
Y Maekawa
L E Benhamou
P Sarthou
T Watanabe
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The HS1 protein is one of the major substrates of non-receptor-type protein-tyrosine kinases and is phosphorylated immediately after crosslinking of the surface IgM on B cells. The mouse B-lymphoma cell line WEHI-231 is known to undergo apoptosis upon crosslinking of surface IgM by anti-IgM antibodies. Variants of WEHI-231 that were resistant to anti-IgM-induced apoptosis expressed dramatically reduced levels of HS1 protein. Expression of the human HS1 protein from an expression vector introduced into one of the variant cell lines restored the sensitivity of the cells to apoptosis induced by surface IgM crosslinking. These results suggest that HS1 protein plays a crucial role in the B-cell antigen receptor-mediated signal transduction pathway that leads to apoptosis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisBlood ProteinsGene ExpressionGenetic VariationHumansImmunoglobulin MLymphoma, B-CellMiceProtein-Tyrosine KinasesReceptors, Antigen, B-CellSignal TransductionSubstrate SpecificityTumor Cells, CulturedAdaptor Proteins, Signal TransducingBlood ProteinsHCLS1 protein, humanImmunoglobulin MProtein-Tyrosine KinasesReceptors, Antigen, B-Cell

Identifiers

PMID7638185
PMCPMC41327
OpenAlexW2054507865

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.