ArticleOncogene1999
Met-induced JNK activation is mediated by the adapter protein Crk and correlates with the Gab1 - Crk signaling complex formation.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Host-pathogen systems biology: logical modelling of hepatocyte growth factor and Helicobacter pylori induced c-Met signal transduction.BMC systems biology · 2008Pooled it
- C-MET tyrosine kinase receptor: mechanisms, clinical applications and future perspectives in cancer therapy.Signal transduction and targeted therapy · 2026Review
- Review
- The Emerging Role of c-Met in Carcinogenesis and Clinical Implications as a Possible Therapeutic Target.Journal of oncology · 2022Review
- Overexpression of CrkL as a novel biomarker for poor prognosis in gastric cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- Activated HGF-c-Met Axis in Head and Neck Cancer.Cancers · 2017Review
- Analysis of progress and challenges for various patterns of c-MET-targeted molecular imaging: a systematic review.EJNMMI research · 2017Review
- Targeting c-MET in gastrointestinal tumours: rationale, opportunities and challenges.Nature reviews. Clinical oncology · 2017Review
- c-Met expression and activity in urogenital cancers - novel aspects of signal transduction and medical implications.Cell communication and signaling : CCS · 2017Review
- JNK Pathway Activation Modulates Acquired Resistance to EGFR/HER2-Targeted Therapies.Cancer research · 2016Article
- c-Met and Other Cell Surface Molecules: Interaction, Activation and Functional Consequences.Biomedicines · 2015Review
- JNK suppression of chemotherapeutic agents-induced ROS confers chemoresistance on pancreatic cancer stem cells.Oncotarget · 2015Article
- CRK SH3N Domain Diminishes Cell Invasiveness of Non-Small Cell Lung Cancer.Genes & cancer · 2013Article
- Protein tyrosine phosphatase-1B regulates the tyrosine phosphorylation of the adapter Grb2-associated binder 1 (Gab1) in the retina.Cell communication and signaling : CCS · 2013Article
- Met receptor tyrosine kinase signals through a cortactin-Gab1 scaffold complex, to mediate invadopodia.Journal of cell science · 2012Article
- An overview of the c-MET signaling pathway.Therapeutic advances in medical oncology · 2011Article
- MET signalling: principles and functions in development, organ regeneration and cancer.Nature reviews. Molecular cell biology · 2010Review
- Function, regulation and pathological roles of the Gab/DOS docking proteins.Cell communication and signaling : CCS · 2009Article
- Crk and CrkL adaptor proteins: networks for physiological and pathological signaling.Cell communication and signaling : CCS · 2009Article
- Gab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor.Molecular biology of the cell · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Constitutive activation of the Met tyrosine kinase results in transformation of cells of diverse origin. Recent studies have demonstrated a role for the c-Jun N-terminal kinase (JNK) in Met-induced transformation, but little is known about the molecular mechanisms that connect Met to JNK activation. Our studies show that activated Met associates with, and phosphorylates, the docking protein Gab1, which in turn binds to the src homology 2 (SH2)-domain of the adapter protein Crk and recruits Crk to the Met signaling complex. Formation of the Gab1 - Crk complex correlates with Met-induced JNK activation, and mutant forms of Met that fail to induce the complex formation also fail to activate JNK. Importantly, expression of a loss-of-function mutant of Crk severely impairs activation of the JNK pathway by Met. We also show here that Met controls the transcription of the matrix metalloproteinase-1 (MMP-1) gene in carcinoma cells and that this transcriptional regulation occurs in a Crk - JNK-dependent manner through an AP-1 element in the MMP-1 promoter. Taken together, our data implicate the Gab1 - Crk signaling complex in Met-induced JNK activation and suggest that the Gab1 - Crk complex formation may be an important event in regulating the tumorigenic phenotype of Met-transformed cells.
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Registered trials
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.