Requirement of Ras-GTP-Raf Complexes for Activation of Raf-1 by Protein Kinase C

Receptor tyrosine kinase-mediated activation of the Raf-1 protein kinase is coupled to the small guanosine triphosphate (GTP)-binding protein Ras. By contrast, protein kinase C (PKC)-mediated activation of Raf-1 is thought to be Ras independent. Nevertheless, stimulation of PKC in COS cells led to a...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1998-04, Vol.280 (5360), p.109-112
Main Authors: Marais, Richard, Light, Yvonne, Mason, Clive, Paterson, Hugh, Olson, Michael F., Marshall, Christopher J.
Format: Article
Language:English
Subjects:
Animals
Antibodies
Biochemistry
Biological and medical sciences
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Carbohydrates
Cell cycle, cell proliferation
Cell extracts
Cell lines
Cell membranes
Cell physiology
Cellular biology
Cercopithecus aethiops
COS Cells
Enzyme Activation
Enzyme Inhibitors - pharmacology
Enzymes
Epidermal Growth Factor - pharmacology
Feedback (Response)
Fundamental and applied biological sciences. Psychology
Guanosine Triphosphate - metabolism
Immunoprecipitation
Individualized Instruction
Indoles - pharmacology
Kidneys
Kinetics
Molecular and cellular biology
Monkeys & apes
Monoclonal antibodies
Mutation
Observations
Protein Kinase C - antagonists & inhibitors
Protein Kinase C - metabolism
Protein kinases
Proteins
Proto-Oncogene Proteins c-raf - genetics
Proto-Oncogene Proteins c-raf - metabolism
ras Proteins - metabolism
Receptor, Muscarinic M1
Receptors
Receptors, Muscarinic - metabolism
Signal Transduction
Tetradecanoylphorbol Acetate - pharmacology
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Summary:Receptor tyrosine kinase-mediated activation of the Raf-1 protein kinase is coupled to the small guanosine triphosphate (GTP)-binding protein Ras. By contrast, protein kinase C (PKC)-mediated activation of Raf-1 is thought to be Ras independent. Nevertheless, stimulation of PKC in COS cells led to activation of Ras and formation of Ras-Raf-1 complexes containing active Raf-1. Raf-1 mutations that prevent its association with Ras blocked activation of Raf-1 by PKC. However, the activation of Raf-1 by PKC was not blocked by dominant negative Ras, indicating that PKC activates Ras by a mechanism distinct from that initiated by activation of receptor tyrosine kinases.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.280.5360.109