ArticleOncogene2000
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.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed, 58 citations in OpenAlex.
- Targeting MET in non-small cell lung cancer brain metastases: from molecular mechanism to precision therapy.Journal of translational medicine · 2026Review
- The Role of GAB1 in Cancer.Cancers · 2023Review
- The Emerging Role of c-Met in Carcinogenesis and Clinical Implications as a Possible Therapeutic Target.Journal of oncology · 2022Review
- BIAM switch assay coupled to mass spectrometry identifies novel redox targets of NADPH oxidase 4.Redox biology · 2019Article
- Fibroblast Growth Requires CT10 Regulator of Kinase (Crk) and Crk-like (CrkL).The Journal of biological chemistry · 2016Article
- Crk II silencing down-regulates IGF-IR and inhibits migration and invasion of prostate cancer cells.Biochemistry and biophysics reports · 2016Article
- c-Met and Other Cell Surface Molecules: Interaction, Activation and Functional Consequences.Biomedicines · 2015Review
- Enhanced prediction of Src homology 2 (SH2) domain binding potentials using a fluorescence polarization-derived c-Met, c-Kit, ErbB, and androgen receptor interactome.Molecular & cellular proteomics : MCP · 2014Article
- Met receptor tyrosine kinase signals through a cortactin-Gab1 scaffold complex, to mediate invadopodia.Journal of cell science · 2012Article
- Models of crk adaptor proteins in cancer.Genes & cancer · 2012Article
- MET signalling: principles and functions in development, organ regeneration and cancer.Nature reviews. Molecular cell biology · 2010Review
- Article
- 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
- MET pathway as a therapeutic target.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2009Review
- MET as a target for treatment of chest tumors.Lung cancer (Amsterdam, Netherlands) · 2009Review
- c-Met is essential for wound healing in the skin.The Journal of cell biology · 2007Article
- Gab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor.Molecular biology of the cell · 2006Article
- Interaction of CagA with Crk plays an important role in Helicobacter pylori-induced loss of gastric epithelial cell adhesion.The Journal of experimental medicine · 2005Article
- Role of Gab1 in UV-induced c-Jun NH2-terminal kinase activation and cell apoptosis.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell transformation is associated with anchorage independent growth and morphological changes characterized by reduced adhesion and spreading. The molecular signals that control these events are poorly understood. The Met receptor tyrosine kinase is deregulated in human tumors and an oncogenic derivative of this receptor transforms cells. In this paper we demonstrate that fibroblasts transformed by the Met oncoprotein display decreased cell spreading consistent with the loss of actin stress fibers and vinculin staining focal adhesions. In contrast to control cells, focal adhesion kinase, p130Cas and paxillin are weakly or not detectably tyrosine phosphorylated in Met transformed cells. Moreover, although paxillin and p130Cas associate with the Crk adapter protein in control cells, they fail to associate with Crk in Met transformed cells, yet these cells are motile and capable of wound closure to the same extent as control cells. In Met transformed cells, Crk predominantly associates with the Cbl and Gab1docking proteins in a tyrosine phosphorylation dependent manner. The coupling of Gab1, but not Cbl, with Crk is retained in cells grown in suspension and enhances JNK activation. We propose that the loss of adhesion dependent signals required for cell cycle progression is compensated through Met induced Gab1/Crk signals.
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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.