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Article

Activation of the JNK pathway is essential for transformation by the Met oncogene.

The EMBO journal - 15 May 1997

Rodrigues G A, Park M, Schlessinger J

Abstract excerpt

The Met/Hepatocyte Growth Factor (HGF) receptor tyrosine kinase is oncogenically activated through a rearrangement that creates a hybrid gene Tpr-Met. The resultant chimeric p65(Tpr-Met) protein is constitutively phosphorylated on tyrosine residues in vivo and associates with a number of SH2-containing signaling molecules including the p85 subunit of PI-3 kinase and the Grb2 adaptor protein, which couples...

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Identifiers

PMID: 9184210
DOI: 10.1093/emboj/16.10.2634
PMCID: PMC1169874

Genes

HGF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Activation of the JNK pathway is essential for transformation by the Met oncogene.PMID 9184210Read ↗

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STK/RON receptor tyrosine kinase mediates both apoptotic and growth signals via the multifunctional docking site conserved among the HGF receptor family.Semantic proximity Read ↗

Cancer therapy: can the challenge be MET?Semantic proximity Read ↗

Suppression of Ras-mediated tumorigenicity and metastasis through inhibition of the Met receptor tyrosine kinaseSemantic proximity Read ↗

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Tumorigenicity of the met proto-oncogene and the gene for hepatocyte growth factor.Semantic proximity Read ↗

A switch from p130Cas/Crk to Gab1/Crk signaling correlates with anchorage independent growth and JNK activation in cells transformed by the Met receptor oncoprotein.Semantic proximity Read ↗

MET: a critical player in tumorigenesis and therapeutic target.Semantic proximity Read ↗

The JNK/SAPK activator mixed lineage kinase 3 (MLK3) transforms NIH 3T3 cells in a MEK-dependent fashion.Semantic proximity Read ↗

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