Met, metastasis, motility and more

No abstract is available for this paper.

• Publication year

  2003

• Venue

  Nature reviews. Molecular cell biology

• Publication date

  2003-12-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/nrm1261PMID 14685170
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Dysregulation of Met receptor tyrosine kinase activity in invasive tumors.

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• CD44 is required for two consecutive steps in HGF/c-Met signaling.

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• Regulation of epithelial cell migration and tumor formation by beta-catenin signaling.

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• Activation of the Met Receptor by Cell Attachment Induces and Sustains Hepatocellular Carcinomas in Transgenic Mice

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• Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways.

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• Hepatocyte growth factor receptor in acute tubular necrosis.

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• Mutation of the c-Cbl TKB domain binding site on the Met receptor tyrosine kinase converts it into a transforming protein.

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• Src Homology 2-containing Inositol 5-Phosphatase 1 Binds to the Multifunctional Docking Site of c-Met and Potentiates Hepatocyte Growth Factor-induced Branching Tubulogenesis*

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• Essential Role of Gab1 for Signaling by the C-Met Receptor in Vivo

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• The geldanamycins are potent inhibitors of the hepatocyte growth factor/scatter factor-met-urokinase plasminogen activator-plasmin proteolytic network.

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• 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

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