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Differential physiological effects of Raf-1 kinase pathways linked to protein kinase C activation depending on the stimulus in v-H-ras-transformed cells.

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Year: 2008 Volume: 40 Issue: 1

Year: 2007 Volume: 39

Year: 2006 Volume: 38

Year: 2005 Volume: 37

Year: 2003 Volume: 35

Year: 2002 Volume: 34

Year: 2001 Volume: 33

Differential physiological effects of Raf-1 kinase pathways linked to protein kinase C activation depending on the stimulus in v-H-ras-transformed cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Michael
Description	Author Affiliation: Lee M ( Department of Biology, College of Natural Sciences, University of Incheon, Incheon, Korea. mikelee@incheon.ac.kr)
Abstract	PURPOSE: We investigated the molecular mechanism by which the Raf-1 kinase pathways that are linked to protein kinase C induce differential physiological effects, depending on the stimulus, by employing the pharmacological PKC activator PMA. MATERIALS AND METHODS: Parental and v-Ha-ras transfected NIH 3T3 cells were chosen as test systems and these cells were transiently transfected with the pMTH vector that encodes dominant-negative (DN) PKC-epsilon with using Lipofectamine 2000. The cell proliferation reagent WST-1 was used for the quantitative determination of cellular proliferation. The Raf-1 kinase activity was measured by assessing the phosphorylation of recombinant MEK with using the immunoprecipitated Raf-1 proteins. The phosphorylated MEK protein bands were quantified by using Quantity One analysis software. RESULTS: The pharmacological PKC activator phorbol-12-myristate-13-acetate (PMA) and platelet-derived growth factor (PDGF) were able to induce the activation of Raf-1 kinase in the v-H-ras-transformed NIH3T3 fibroblasts. However, PMA was found to be much less sensitive PI3 kinase inhibitor or the chemical antioxidant than is PDGF. Especially, PMA mediated growth arrest while PDGF induced mitogenic signaling through the PKC-epsilon activation. Thus, the regulation of the Raf-1 cascade by both PDGF and PMA is likely to be intimately linked and they converge at the PKC level through different upstream pathways, as was shown by the inhibition of PDGF-induced Raf-1 kinase activation by the transient transfection with a dominant-negative mutant of PKC-epsilon. CONCLUSIONS: Taken together, these results imply that, depending on the stimulus, Raf-1 kinase leads to different physiological effects.
File Format	HTM / HTML
ISSN	15982998
e-ISSN	20059256
DOI	10.4143/crt.2008.40.2.39
Journal	Cancer Research and Treatment
Issue Number	2
Volume Number	40
Language	English
Publisher	Korean Cancer Association.
Publisher Date	2008-06-01
Publisher Place	Korea (South)
Access Restriction	Open
Subject Keyword	Discipline Neoplasms
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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Differential Physiological Effects of Raf-1 Kinase Pathways Linked to Protein Kinase C Activation Depending on the Stimulus in v-H-ras-transformed Cells

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Differential physiological effects of Raf-1 kinase pathways linked to protein kinase C activation depending on the stimulus in v-H-ras-transformed cells.

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