Affiliation:
1. Howard Hughes Medical Institute, Department of Biochemistry, New York University Medical Center, New York 10016.
Abstract
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.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology