Altered transcriptional activity of c-fos promoter plasmids in v-raf-transformed NIH 3T3 cells.

AUTOR(ES)

Siegfried, Z

RESUMO

In cells transformed by v-raf, an oncogenic counterpart of the serine/threonine kinase Raf-1, regulatory elements of the c-fos promoter were active under conditions of cell growth or stimulation for which they were inactive in untransformed control cells. This suggests that v-raf transforms by deregulating transcription of early response genes.

Documentos Relacionados

• The Mos/MAP kinase pathway stabilizes c-Fos by phosphorylation and augments its transforming activity in NIH 3T3 cells.
• Antisense RNA of proto-oncogene c-fos blocks renewed growth of quiescent 3T3 cells.
• Platelet-derived growth factor does not induce c-fos in NIH 3T3 cells expressing the EJ-ras oncogene.
• Inducible production of c-fos antisense RNA inhibits 3T3 cell proliferation.
• Novel Membrane-Targeted ERK1 and ERK2 Chimeras Which Act as Dominant Negative, Isotype-Specific Mitogen-Activated Protein Kinase Inhibitors of Ras-Raf-Mediated Transcriptional Activation of c-fos in NIH 3T3 Cells