Evidence map›Paper›PMID 11094067›Full record

ArticleMolecular and cellular biology2000

Pleiotropic contributions of phospholipase C-gamma1 (PLC-gamma1) to T-cell antigen receptor-mediated signaling: reconstitution studies of a PLC-gamma1-deficient Jurkat T-cell line.

B J Irvin, B L Williams, A E Nilson, H O Maynor, R T Abraham

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

56 citing papers in PubMed, 124 citations in OpenAlex.

  1. T cell CaFrontiers in immunology · 2023
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  5. Functions of NKG2D in CD8Cellular & molecular immunology · 2018
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  14. Impact of Alcohol Abuse on the Adaptive Immune System.Alcohol research : current reviews · 2015
    Review
  15. Article
  16. Article
  17. VDR hypermethylation and HIV-induced T cell loss.Journal of leukocyte biology · 2013
    Article
  18. Ethanol and vitamin D receptor in T cell apoptosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Article
  19. Article
  20. Article
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

5 authors at 3 institutions in 2 countries.

B J IrvinDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
B L Williams
A E Nilson
H O Maynor
R T Abraham
Duke Medical Center · USMayo Clinic · USUniversity of Cambridge · GB

Funding

SIGNAL TRANSDUCTION FROM THE T-CELL ANTIGEN RECEPTORR01GM047286 · NIGMS · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI ABRAHAM, ROBERT T · 1992 to 2003
$1.3M
NIGMS NIH HHS GM47286NIGMS NIH HHS R01 GM047286Wellcome Trust
6 · The paper itself

Abstract

Phospholipase C-gamma1 (PLC-gamma1) plays a crucial role in the coupling of T-cell antigen receptor (TCR) ligation to interleukin-2 (IL-2) gene expression in activated T lymphocytes. In this study, we have isolated and characterized two novel, PLC-gamma1-deficient sublines derived from the Jurkat T-leukemic cell line. The P98 subline displays a >90% reduction in PLC-gamma1 expression, while the J.gamma1 subline contains no detectable PLC-gamma1 protein. The lack of PLC-gamma1 expression in J.gamma1 cells caused profound defects in TCR-dependent Ca(2+) mobilization and NFAT activation. In contrast, both of these responses occurred at normal levels in PLC-gamma1-deficient P98 cells. Unexpectedly, the P98 cells displayed significant and selective defects in the activation of both the composite CD28 response element (RE/AP) and the full-length IL-2 promoter following costimulation with anti-TCR antibodies and phorbol ester. These transcriptional defects were reversed by transfection of P98 cells with a wild-type PLC-gamma1 expression vector but not by expression of mutated PLC-gamma1 constructs that lacked a functional, carboxyl-terminal SH2 [SH2(C)] domain or the major Tyr(783) phosphorylation site. On the other hand, the amino-terminal SH2 [SH2(N)] domain was not essential for reconstitution of RE/AP- or IL-2 promoter-dependent transcription but was required for the association of PLC-gamma1 with LAT, as well as the tyrosine phosphorylation of PLC-gamma1 itself, in activated P98 cells. These studies demonstrate that the PLC-gamma1 SH2(N) and SH2(C) domains play functionally distinct roles during TCR-mediated signaling and identify a non-Ca(2+)-related signaling function linked to the SH2(C) domain, which couples TCR plus phorbol ester-CD28 costimulation to the activation of the IL-2 promoter in T lymphocytes.

Indexed as

Adaptor Proteins, Signal TransducingMembrane ProteinsNuclear ProteinsCalciumCarrier ProteinsDNA-Binding ProteinsGenes, ReporterHumansImmunosuppressive AgentsInterleukin-2IsoenzymesJurkat CellsLymphocyte ActivationMuromonab-CD3MutagenesisNFATC Transcription FactorsAdaptor Proteins, Signal TransducingCalciumCarrier ProteinsDNA-Binding ProteinsImmunosuppressive AgentsInterleukin-2IsoenzymesLAT protein, humanMembrane ProteinsMuromonab-CD3NFATC Transcription FactorsNuclear ProteinsPhospholipase C gammaPhosphoproteinsProtein-Tyrosine KinasesReceptors, Antigen, T-CellTetradecanoylphorbol AcetateTranscription FactorsType C Phospholipases

Identifiers

PMID11094067
PMCPMC102173
OpenAlexW2138751131

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.