Evidence map›Paper›PMID 12032773›Full record

ReviewOncogene2002

JAKs, STATs and Src kinases in hematopoiesis.

Sushil G Rane, E Premkumar Reddy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Article
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  13. Targeted Sequencing Identifies the Genetic Variants Associated with High-altitude Polycythemia in the Tibetan Population.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2022
    Article
  14. Article
  15. Article
  16. Review
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  18. Article
  19. Article
  20. Review

17 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sushil G RaneLaboratory of Cell Regulation & Carcinogenesis, NCI, NIH, Bldg. 41, C629, 41 Library Drive, Bethesda, Maryland, MD 20892, USA.
E Premkumar Reddy
Temple University · US

Funding

AATYK--A NOVEL APOPTOSIS ASSOCIATED TYROSINE KINASER01ES009225 · NIEHS · TEMPLE UNIVERSITY · PI REDDY, E PREMKUMAR · 1998 to 2002
$699k
NIEHS NIH HHS ES09225
6 · The paper itself

Abstract

Hematopoiesis is the cumulative result of intricately regulated signal transduction cascades that are mediated by cytokines and their cognate receptors. Proper culmination of these diverse signaling pathways forms the basis for an orderly generation of different cell types and aberrations in these pathways is an underlying cause for diseases such as leukemias and other myeloproliferative and lymphoproliferative disorders. Over the past decade, downstream signal transduction events initiated upon cytokine/growth factor stimulation have been a major focus of basic and applied biomedical research. As a result, several key concepts have emerged allowing a better understanding of the complex signaling processes. A group of transcription factors, termed signal transducers and activators of transcription (STATs) appear to orchestrate the downstream events propagated by cytokine/growth factor interactions with their cognate receptors. Similarly, cytoplasmic Janus protein tyrosine kinases (JAKs) and Src family of kinases seem to play a critical role in diverse signal transduction pathways that govern cellular survival, proliferation, differentiation and apoptosis. Accumulating evidence suggests that STAT protein activation may be mediated by members of both JAK and Src family members following cytokine/growth factor stimulation. In addition, JAK kinases appear to be essential for the phosphorylation of the cytokine receptors which results in the creation of docking sites on the receptors for binding of SH2-containing proteins such as STATs, Src-kinases and other signaling intermediates. Cell and tissue-specificity of cytokine action appears to be determined by the nature of signal transduction pathways activated by cytokine/receptor interactions. The integration of these diverse signaling cues from active JAK kinases, members of the Src-family kinases and STAT proteins, leads to cell proliferation, cell survival and differentiation, the end-point of the cytokine/growth factor stimulus.

Indexed as

AnimalsApoptosisCell DivisionCloning, MolecularCytokinesDNA-Binding ProteinsHematopoiesisHumansJanus Kinase 1Models, BiologicalPhosphorylationProtein-Tyrosine KinasesSignal Transductionsrc-Family KinasesSTAT1 Transcription FactorTrans-ActivatorsCytokinesDNA-Binding ProteinsJAK1 protein, humanJanus Kinase 1Protein-Tyrosine Kinasessrc-Family KinasesSTAT1 protein, humanSTAT1 Transcription FactorTrans-Activators

Identifiers

PMID12032773
OpenAlexW1980814049

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.