Evidence map›Paper›PMID 17266928›Full record

ArticleBiochemical and biophysical research communications2007

Cell type-specific roles of Jak3 in IL-2-induced proliferative signal transduction.

Hodaka Fujii

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Hodaka FujiiDepartment of Pathology, New York University School of Medicine, 550 First Avenue, MSB-126, New York, NY 10016, USA. hodaka@med.nyu.edu
New York University · US

Funding

Cytokine signal transduction in immune systemR01AI059315 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FUJII, HODAKA · 2005 to 2007
$989k
NIAID NIH HHS R01 AI059315NIAID NIH HHS R01 AI059315-01A1NIAID NIH HHS R01 AI059315-02NIAID NIH HHS R01 AI059315-03
6 · The paper itself

Abstract

Binding of interleukin-2 (IL-2) to its specific receptor induces activation of two members of Jak family protein tyrosine kinases, Jak1 and Jak3. An IL-2 receptor (IL-2R)-reconstituted NIH 3T3 fibroblast cell line proliferates in response to IL-2 only when hematopoietic lineage-specific Jak3 is ectopically expressed. However, the mechanism of Jak3-dependent proliferation in the fibroblast cell line is not known. Here, I showed that Jak3 expression is dispensable for IL-2-induced activation of Jak1 and Stat proteins and expression of nuclear proto-oncogenes in the IL-2R-reconstituted fibroblast cell line. Jak3 expression markedly enhanced these IL-2-induced signaling events. In contrast, Jak3 expression was essential for induction of cyclin genes involved in the G1-S transition. These data suggest a critical role of Jak3 in IL-2 signaling in the fibroblast cell line and may provide further insight into the cell type-specific mechanism of cytokine signaling.

Indexed as

AnimalsBinding SitesCell ProliferationCyclinsCytokinesFibroblastsG1 PhaseInterleukin-2Janus Kinase 1Janus Kinase 3MiceNIH 3T3 CellsSignal TransductionS PhaseSTAT Transcription FactorsCyclinsCytokinesInterleukin-2Janus Kinase 1Janus Kinase 3STAT Transcription Factors

Identifiers

PMID17266928
PMCPMC1839827
OpenAlexW2017320436

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.