Evidence map›Paper›PMID 9120025›Full record

ArticleThe Journal of clinical investigation1997

Cytokine signaling through the novel tyrosine kinase RAFTK in Kaposi's sarcoma cells.

Z Y Liu, R K Ganju, J F Wang, M A Ona, W C Hatch, T Zheng, S Avraham, P Gill, J E Groopman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Selective adapter recruitment and differential signaling networks by VEGF vs. shear stress.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Lymphagenesis and cancer metastasis.British journal of cancer · 1998
    Article
  12. Article
  13. Article
  14. 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

9 authors at 3 institutions in 1 country.

Z Y LiuDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
R K Ganju
J F Wang
M A Ona
W C Hatch
T Zheng
S Avraham
P Gill
J E Groopman
Harvard University · USBeth Israel Deaconess Medical Center · USUniversity of Southern California · US

Funding

PATHOBIOLOGY OF HIV SUPPRESSION OF HEMATOPOIESISR01HL053745 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GROOPMAN, JEROME E · 1994 to 2004
$2.1M
THE MACROPHAGE MANNOSE RECEPTOR IN PNEUMOCYSTIS CARINII INFECTIONP01HL043510 · NHLBI · NEW ENGLAND DEACONESS HOSPITAL · PI HARMSEN, ALLEN G · 1989 to 1998
–
THROMBOPOIETIN FOR AIDS RELATED THROMBOCYTOPOIESISR01HL055187 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GROOPMAN, JEROME E · 1995 to 1998
–
NHLBI NIH HHS HL-43510-07NHLBI NIH HHS HL-53745-02NHLBI NIH HHS HL-55187-01
6 · The paper itself

Abstract

A number of cytokines, including basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), oncostatin M (OSM), IL-6, and tumor necrosis factor alpha (TNF-alpha), have been postulated to have a role in the pathogenesis of Kaposi's sarcoma (KS). The proliferative effects of bFGF and OSM may be via their reported activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway in KS cells. We now report that KS cells express a recently identified focal adhesion kinase termed RAFTK which appears in other cell systems to coordinate surface signals between cytokine and integrin receptors and the cytoskeleton as well as act downstream to modulate JNK activation. We also report that the tyrosine kinase receptor FLT-4, present on normal lymphatic endothelium, is robustly expressed in KS cells. Treatment of KS cells with VEGF-related protein (VRP), the ligand for the FLT-4 receptor, as well as with the cytokines bFGF, OSM, IL-6, VEGF, or TNF-alpha resulted in phosphorylation and activation of RAFTK. Following its activation, there was an enhanced association of RAFTK with the cytoskeletal protein paxillin. This association was mediated by the hydrophobic COOH-terminal domain of the kinase. Furthermore, JNK activity was increased in KS cells after VEGF or VRP stimulation. We postulate that in these tumor cells RAFTK may be activated by a diverse group of stimulatory cytokines and facilitate signal transduction to the cytoskeleton and downstream to the growth promoting JNK pathway.

Indexed as

JNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase KinasesAnimalsCytokinesCytoskeletal ProteinsFocal Adhesion Kinase 2HumansMAP Kinase Kinase 4PaxillinPhosphoproteinsPhosphorylationProtein KinasesProtein-Tyrosine KinasesRabbitsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorCytokinesCytoskeletal ProteinsFocal Adhesion Kinase 2JNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Mitogen-Activated Protein Kinase KinasesPaxillinPhosphoproteinsProtein KinasesProtein-Tyrosine KinasesPXN protein, humanReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth Factor

Identifiers

PMID9120025
PMCPMC508001
OpenAlexW2024976039

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.