P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor.
AUTOR(ES)
Zullo, J N
RESUMO
The viral oncogene v-ras inhibited the platelet-derived growth factor (PDGF)-induced upregulation of c-myc and c-fos proto-oncogene expression in fibroblast monolayers. These v-ras-containing cells proliferated in the absence of c-myc induction and no longer required PDGF to support growth. Fibroblasts expressing v-ras continued to express the same number of functional PDGF receptors on their surface as uninfected cells, yet the usual induction of transcription of the genes c-myc, c-fos, and JE in response to PDGF stimulation did not occur in the presence of newly introduced v-ras or chronic v-ras gene expression, and synthesis of c-myc protein did not occur. This inhibitory effect on growth factor-mediated induction of cellular proto-oncogenes was specific for PDGF in that induction of the c-myc and c-fos genes by certain other factors was not impaired.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=365609Documentos Relacionados
- Platelet-derived growth factor does not induce c-fos in NIH 3T3 cells expressing the EJ-ras oncogene.
- Heparin inhibits c-fos and c-myc mRNA expression in vascular smooth muscle cells.
- Induction of c-fos and c-myc mRNA by epidermal growth factor or calcium ionophore is cAMP dependent.
- Protein kinase PKR is required for platelet-derived growth factor signaling of c-fos gene expression via Erks and Stat3
- Induction of platelet-derived growth factor A-chain and c-myc gene expressions by angiotensin II in cultured rat vascular smooth muscle cells.