Evidence map›Paper›PMID 19290928›Full record

ReviewImmunological reviews2009

Calmodulin-dependent phosphatase, kinases, and transcriptional corepressors involved in T-cell activation.

Jun O Liu

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 83 citations in OpenAlex.

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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.

Jun O LiuDepartment of Pharmacology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. joliu@jhu.edu
Johns Hopkins University · US

Funding

SIGNAL TRANSDUCTION BY CALCINEURIN IN T LYMPHOCYTESR01GM055783 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LIU, JUN O. · 1997 to 2003
$367k
NIGMS NIH HHS R01 GM055783
6 · The paper itself

Abstract

The second messenger calcium plays an essential role in mediating the T-cell receptor (TCR) signaling pathway leading to cytokine production and T-cell clonal expansion. The immunosuppressive drugs cyclosporine A and FK506 have served both as therapeutic agents and as molecular probes for unraveling the protein phosphatase calcineurin as a rate-limiting enzyme involved in the transmission of calcium signal from the cytosol into the nucleus to reprogram gene expression. The use of mouse knockout models has helped to verify and further elucidate the functions of different isoforms of calcineurin in both helper T-cell activation and thymocyte development. In addition to calcineurin, three other classes of calmodulin-binding proteins have also been shown to play important roles in calcium signaling in T cells. Thus, Cabin1 and class II histone deacetylases have been found to constitute a novel calcium-signaling module in conjunction with the transcription factor myocyte enhance factor family and the transcriptional coactivator p300 to suppress and activate cytokine gene transcription in a calcium-dependent manner. The calmodulin-dependent protein kinases II and IV were also shown to play negative and positive regulatory functions, respectively, in TCR-mediated cytokine production. The crosstalks among these and other signal transducers in T cells form an extensive nonlinear signaling network that dictates the final outcome of the TCR signaling pathway.

Indexed as

Lymphocyte ActivationAnimalsCalcineurinCalciumCalmodulinHumansT-LymphocytesCalcineurinCalciumCalmodulin

Identifiers

PMID19290928
PMCPMC2669740
OpenAlexW1997671040

What OpenQuestion holds

Textmetadata
LicenceTDM
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.