Evidence map›Paper›PMID 11339369›Full record

ReviewImmunologic research2000

Mutant T cell lines as model systems for the dissection of T cell antigen receptor signaling pathways.

R T Abraham

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-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

4 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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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

1 author at 1 institution in 1 country.

R T AbrahamDepartment of Pharmacology and Cancer Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
Duke University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cell antigen receptor (TCR) ligation triggers a cascade of intracellular signaling events that culminate in T cell activation, cytokine gene expression, differentiation, or apoptosis. Many of the enzymes and adapter proteins responsible for signal propagation from the cell surface TCR to the cytoplasm and nucleus have now been identified and molecularly cloned. However, a comprehensive understanding of the regulation and functions of these signaling proteins in T cells remains a major challenge. Our laboratory has approached this problem through the generation of a panel of Jurkat T cell-derived somatic mutants that fail to express several critical elements in the TCR-linked signaling cascade. This review highlights the use of mutant T cell lines for functional characterizations of two of these signaling proteins--the ZAP-70 tyrosine kinase and phospholipase C-gamma1.

Indexed as

Signal TransductionAnimalsHumansIsoenzymesJurkat CellsLymphocyte ActivationMutationPhospholipase C gammaProtein-Tyrosine KinasesReceptors, Antigen, T-CellT-LymphocytesType C PhospholipasesZAP-70 Protein-Tyrosine KinaseIsoenzymesPhospholipase C gammaProtein-Tyrosine KinasesReceptors, Antigen, T-CellType C PhospholipasesZAP70 protein, humanZAP-70 Protein-Tyrosine Kinase

Identifiers

PMID11339369
OpenAlexW2033597395

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.