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Craig P. Webb

Researcher at Van Andel Institute

Publications -  60
Citations -  4443

Craig P. Webb is an academic researcher from Van Andel Institute. The author has contributed to research in topics: Cancer & Metastasis. The author has an hindex of 29, co-authored 60 publications receiving 4276 citations.

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Proteolytic Inactivation of MAP-Kinase-Kinase by Anthrax Lethal Factor

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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Activating mutations for the Met tyrosine kinase receptor in human cancer

TL;DR: The results demonstrate that the Met mutants originally identified in human papillary renal carcinoma are oncogenic and thus are likely to play a determinant role in this disease, and raise the possibility that activating Met mutations also may contribute to other human malignancies.
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Renal biomarker qualification submission: a dialog between the FDA-EMEA and Predictive Safety Testing Consortium

Frank Dieterle, +68 more
- 01 May 2010 - 
TL;DR: This was a pilot process, and the experience gained will both facilitate better understanding of how the qualification process will probably evolve and clarify the minimal requirements necessary to evaluate the performance of biomarkers of organ injury within specific contexts.
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The mutationally activated Met receptor mediates motility and metastasis

TL;DR: It is found that mutant Met induces the motility of Madin-Darby canine kidney cells in vitro and experimental metastasis of NIH 3T3 cells in vivo, and that the Ras-Raf-MEK-ERK signaling pathway, which has been implicated previously in cellular motility and metastasis, is constitutively activated by the Met mutants.
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Signaling pathways in Ras-mediated tumorigenicity and metastasis

TL;DR: Results show that the metastatic properties of the Ras effector domain mutants segregate, and that, whereas Ras-mediated tumorigenicity can arise independently of ERK1/2 activation, experimental metastasis appears to require constitutive activation of the ERK 1/2 pathway.