ArticleMolecular and cellular biology2004
Proapoptotic function of the MET tyrosine kinase receptor through caspase cleavage.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 101 citations in OpenAlex.
- Research progress on resistance and mechanisms of c-Met inhibitors in treatingJournal of thoracic disease · 2026Review
- Article
- Autoregulation of the MET receptor tyrosine kinase by its intracellular juxtamembrane domain.The Biochemical journal · 2025Article
- Comprehensive map of the regulatory network triggered by MET exon 14 skipping reveals important involvement of the RAS-ERK signaling pathway.Cell death & disease · 2025Article
- Mechanistic insights into MET exon 14 skipping mutations and their role in tumor progression.Biochemical Society transactions · 2025Review
- Development of a cyst-targeted therapy for polycystic kidney disease using an antagonistic dimeric IgA monoclonal antibody against cMET.Cell reports. Medicine · 2025Article
- Review
- Article
- Review
- MET exon 14 skipping mutation is a hepatocyte growth factor (HGF)-dependent oncogenic driver in vitro and in humanised HGF knock-in mice.Molecular oncology · 2023Article
- Caspase Cleavage of Receptor Tyrosine Kinases in the Dependence Receptor Family.Biomolecules & therapeutics · 2023Review
- Combination of Type I and Type II MET Tyrosine Kinase Inhibitors as Therapeutic Approach to Prevent Resistance.Molecular cancer therapeutics · 2022Article
- Dependence receptors: new targets for cancer therapy.EMBO molecular medicine · 2021Review
- When the MET receptor kicks in to resist targeted therapies.Oncogene · 2021Review
- Proteolytic Cleavage of Receptor Tyrosine Kinases.Biomolecules · 2021Review
- Strategies to better treat glioblastoma: antiangiogenic agents and endothelial cell targeting agents.Future medicinal chemistry · 2021Review
- MET ectodomain shedding is associated with poor disease-free survival of patients diagnosed with oral squamous cell carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Molecular Engineering Strategies Tailoring the Apoptotic Response to a MET Therapeutic Antibody.Cancers · 2020Article
- Proteolytic cleavages of MET: the divide-and-conquer strategy of a receptor tyrosine kinase.BMB reports · 2019Review
- Anaplastic Lymphoma Kinase (ALK) Receptor Tyrosine Kinase: A Catalytic Receptor with Many Faces.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MET tyrosine kinase, the receptor of hepatocyte growth factor-scatter factor (HGF/SF), is known to be essential for normal development and cell survival. We report that stress stimuli induce the caspase-mediated cleavage of MET in physiological cellular targets, such as epithelial cells, embryonic hepatocytes, and cortical neurons. Cleavage occurs at aspartic residue 1000 within the SVD site of the juxtamembrane region, independently of the crucial docking tyrosine residues Y1001 or Y1347 and Y1354. This cleavage generates an intracellular 40-kDa MET fragment containing the kinase domain. The p40 MET fragment itself causes apoptosis of MDCK epithelial cells and embryonic cortical neurons, whereas its kinase-dead version is impaired in proapoptotic activity. Finally, HGF/SF treatment does not favor MET cleavage and apoptosis, confirming the known survival role of ligand-activated MET. Our results show that stress stimuli convert the MET survival receptor into a proapoptotic factor.
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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.