CDC25(Mm)/Ras-GRF1 regulates both Ras and Rac signaling pathways
| Autor: | Metello Innocenti, Renata Zippel, Emmapaola Sturani, Riccardo Brambilla |
|---|---|
| Přispěvatelé: | Innocenti, M, Zippel, R, Brambilla, R, Sturani, E |
| Rok vydání: | 1999 |
| Předmět: |
MAPK/ERK pathway
Transcription Genetic Mutant Biophysics Biology Transfection Biochemistry Homology (biology) c-Jun NH2-terminal kinase chemistry.chemical_compound Mice Ras-GRF1 Structural Biology Lysophosphatidic acid Genetics Animals Molecular Biology Ra Models Genetic Kinase ras-GRF1 JNK Mitogen-Activated Protein Kinases Cell Biology 3T3 Cells Molecular biology Rac Up-Regulation rac GTP-Binding Proteins Pleckstrin homology domain External stimuli-regulated kinase chemistry Gene Expression Regulation Mutagenesis COS Cells ras Proteins Signal transduction Lysophospholipids Mitogen-Activated Protein Kinases Proto-Oncogene Proteins c-fos Ras Plasmids Signal Transduction |
| Zdroj: | FEBS letters. 460(2) |
| ISSN: | 0014-5793 |
| Popis: | The Ras-GRF1 exchange factor molecule contains in addition to the catalytic domain two pleckstrin homology (PH1 and PH2), one IQ and one Dbl homology (DH) domains. In this study we investigated the role of such additional domains. We found that a Ras-GRF1 mutant lacking PH1 and IQ domains is sufficient to activate c-fos promoter in response to lysophosphatidic acid (LPA). The same mutant did not increase external stimuli-regulated kinase (ERK) activity, suggesting an additional mechanism for the induction of gene transcription. Isolated DH-PH2 module activates c-Jun NH2-terminal kinase and the c-fos promoter in response to LPA, providing the basis for an ERK-independent mechanism. These results provide evidence that Ras-GRF1 acts as a bifunctional molecule on both ERK-dependent and independent pathways. |
| Databáze: | OpenAIRE |
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