Evidence map›Paper›PMID 9799234›Full record

ArticleThe EMBO journal1998

Kit signaling through PI 3-kinase and Src kinase pathways: an essential role for Rac1 and JNK activation in mast cell proliferation.

I Timokhina, H Kissel, G Stella, P Besmer

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  10. Noncoding RNAs in Drug Resistance of Gastrointestinal Stromal Tumor.Frontiers in cell and developmental biology · 2022
    Review
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  17. Deficiency in Fpr2 results in reduced numbers of LinThe Journal of biological chemistry · 2018
    Article
  18. Article
  19. Direct engagement of the PI3K pathway by mutant KIT dominates oncogenic signaling in gastrointestinal stromal tumor.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. Article

36 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

4 authors at 2 institutions in 1 country.

I TimokhinaMolecular Biology Program, Memorial Sloan-Kettering Cancer Center, Cornell University Graduate School of Medical Sciences, New York, NY 10021, USA.
H Kissel
G Stella
P Besmer
Cornell University · USMemorial Sloan Kettering Cancer Center · US

Funding

PI 3-KINASE AND KIT RECEPTOR SIGNALINGR01HL055748 · NHLBI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BESMER, PETER · 1997 to 2012
$4.0M
NORMAL FUNCTION AND ONCOGENIC ACTIVATIONR37CA032926 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BESMER, PETER · 1991 to 1998
–
NCI NIH HHS R37 CA32926NHLBI NIH HHS HL/DK55748
6 · The paper itself

Abstract

The receptor tyrosine kinase Kit plays critical roles in hematopoiesis, gametogenesis and melanogenesis. In mast cells, Kit receptor activation mediates several cellular responses including cell proliferation and suppression of apoptosis induced by growth factor deprivation and gamma-irradiation. Kit receptor functions are mediated by kinase activation, receptor autophosphorylation and association with various signaling molecules. We have investigated the role of phosphatidylinositol 3'-kinase (PI 3-kinase) and Src kinases in Kit-mediated cell proliferation and suppression of apoptosis induced both by factor deprivation and irradiation in bone marrow-derived mast cells (BMMC). Analysis of Kit-/- BMMC expressing mutant Kit receptors and the use of pharmacological inhibitors revealed that both signaling pathways contribute to these Kit-mediated responses and that elimination of both pathways abolishes them. We demonstrate that the PI 3-kinase and Src kinase signaling pathways converge to activate Rac1 and JNK. Analysis of BMMC expressing wild-type and dominant-negative mutant forms of Rac1 and JNK revealed that the Rac1/JNK pathway is critical for Kit ligand (KL)-induced proliferation of mast cells but not for suppression of apoptosis. In addition, KL was shown to inhibit sustained activation of JNK induced by gamma-irradiation and concomitant irradiation-induced apoptosis.

Indexed as

Mitogen-Activated Protein KinasesAnimalsApoptosisCalcium-Calmodulin-Dependent Protein KinasesCell DivisionEnzyme ActivationGTP-Binding ProteinsJNK Mitogen-Activated Protein KinasesMast CellsMiceMice, Inbred StrainsMutationPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-kitrac GTP-Binding ProteinsCalcium-Calmodulin-Dependent Protein KinasesGTP-Binding ProteinsJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-kitrac GTP-Binding Proteinssrc-Family KinasesStem Cell Factor

Identifiers

PMID9799234
PMCPMC1170951
OpenAlexW2163190642

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.