Mouse JunD negatively regulates fibroblast growth and antagonizes transformation by ras.
As NIH 3T3 fibroblasts become quiescent, the level of c-Jun protein decreases while JunD accumulates. When resting cells are stimulated with fresh serum, nuclear-localized JunD is rapidly degraded, followed by resynthesis of both c-Jun and JunD later in G1. Overexpression of JunD results in slower growth and an increase in the percentage of cells in G0/G1 while c-Jun overexpression produces larger S/G2 and M phase populations. In addition, JunD partially suppresses transformation by an activated ras gene whereas c-Jun cooperates with ras to transform cells. These data indicate that two closely related transcription factors can function in an opposing manner.
Pfarr
C M
CM
Département des Biotechnologies, Institut Pasteur, Paris, France.
Mechta
F
F
Spyrou
G
G
Lallemand
D
D
Carillo
S
S
Yaniv
M
M
D000595:Amino Acid Sequence; D000818:Animals; D002453:Cell Cycle; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D005347:Fibroblasts / Q000166:cytology; D011905:Genes, ras; D051379:Mice; D008969:Molecular Sequence Data; D010455:Peptides / Q000737:chemistry; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics* / Q000378:metabolism
D010455:Peptides; D016755:Proto-Oncogene Proteins c-jun