G
George F. Vande Woude
Researcher at Van Andel Institute
Publications - 157
Citations - 21565
George F. Vande Woude is an academic researcher from Van Andel Institute. The author has contributed to research in topics: Hepatocyte growth factor & Receptor tyrosine kinase. The author has an hindex of 68, co-authored 157 publications receiving 20751 citations. Previous affiliations of George F. Vande Woude include Litton Industries.
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Met, metastasis, motility and more
TL;DR: Pivotal roles for Met in development and cancer have been established: Met controls cell migration and growth in embryogenesis; it also controls growth, invasion and metastasis in cancer cells; and activating Met mutations predispose to human cancer.
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Targeting MET in cancer: rationale and progress
TL;DR: Progress in understanding the structure and function of HGF/SF, MET and associated signalling components has led to the successful development of blocking antibodies and a large number of small-molecule MET kinase inhibitors, as well as results from recent clinical studies that demonstrate that inhibiting MET signalling in several types of solid human tumours has major therapeutic value.
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Proteolytic Inactivation of MAP-Kinase-Kinase by Anthrax Lethal Factor
Nicholas S. Duesbery,Craig P. Webb,Stephen H. Leppla,Valery M. Gordon,Kurt Klimpel,Terry D. Copeland,Natalie G. Ahn,M Oskarsson,Kenji Fukasawa,Ken D. Paull,George F. Vande Woude +10 more
TL;DR: It is shown that LF is a protease that cleaves the amino terminus of mitogen-activated protein kinase kinases 1 and 2 and that this cleavage inactivates MAPKK1 and inhibits the MAPK signal transduction pathway.
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Molecular cloning of a new transforming gene from a chemically transformed human cell line
Colin Cooper,Morag Park,Donald G. Blair,Michael A. Tainsky,Kay Huebner,Carlo M. Croce,George F. Vande Woude +6 more
TL;DR: Molecular cloning of the transforming gene from a chemically transformed human osteosarcoma-derived cell line enables the gene to be mapped to chromosome 7 (7p11.4–7qter) and by direct hybridization to be shown to be unrelated to known oncogenes.
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Abnormal Centrosome Amplification in the Absence of p53
TL;DR: In mouse embryonic fibroblasts lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle, implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.