Nucleic Acids Research, 1991, Vol. 19, No. 7 1585-1591
© 1991
MOLECULAR BIOLOGY |
Transcriptional control of c-jun by retinoic acid
Hubrecht Laboratory, Netherlands Institute for Developmental Biology Uppsalalaan 8, 3584 CT Utrecht, The Netherlands
* To whom correspondence should be addressed
Received December 5, 1990. Revised March 4, 1991. Accepted March 4, 1991.
The proto-oncogene c-jun, a major component of transcription factor AP-1, is expressed at very low levels in undifferentiated embryonal carcinoma (EC) end embryonic stem (ES) cells. Retinoic acid (RA) induced differentiation causes a strong increase in the levels of c-jun mRNA. In this paper we report the cloning and characterization of the mouse c-jun promoter. Our results show that RA treatment causes a strong enhancement in c-jun promoter activity, an effect probably mediated by the RA-receptor ß (RARß). Sequences located between –329 and –293 are responsible for the observed RA effect, and bind at least five different protein complexes, of which three are decreased upon RA treatment. These protein binding sites do not resemble RA-responsive elements (RARE's) found in the promoters of retinoic acid receptor ß (RARß) and laminin B1. Furthermore, we could not detect a direct interaction of RAR
and RARß to these sequences, indicating that RA-induced c-jun expression is an indirect effect of RAR action.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  W. Hipkaeo, T. Wakayama, M. Yamamoto, and S. Iseki Expression and Localization of the Transcription Factor JunD in the Duct System of Mouse Submandibular Gland J. Histochem. Cytochem., April 1, 2004; 52(4): 479 - 490. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. LUCIO-CAZANA, K. NAKAYAMA, Q. XU, T. KONTA, V. MORENO-MANZANO, A. FURUSU, and M. KITAMURA Suppression of Constitutive but Not IL-1{beta}-Inducible Expression of Monocyte Chemoattractant Protein-1 in Mesangial Cells by Retinoic Acids: Intervention in the Activator Protein-1 Pathway J. Am. Soc. Nephrol., April 1, 2001; 12(4): 688 - 694. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Moreno-Manzano, Y. Ishikawa, J. Lucio-Cazana, and M. Kitamura Suppression of Apoptosis by All-trans-Retinoic Acid. DUAL INTERVENTION IN THE c-JUN N-TERMINAL KINASE-AP-1 PATHWAY J. Biol. Chem., July 16, 1999; 274(29): 20251 - 20258. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Marinissen, M. Chiariello, M. Pallante, and J. S. Gutkind A Network of Mitogen-Activated Protein Kinases Links G Protein-Coupled Receptors to the c-jun Promoter: a Role for c-Jun NH2-Terminal Kinase, p38s, and Extracellular Signal-Regulated Kinase 5 Mol. Cell. Biol., June 1, 1999; 19(6): 4289 - 4301. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. B. van Dijk, E. Caldenhoven, J. A.M. Raaijmakers, J.-W. J. Lammers, L. Koenderman, and R. P. de Groot The Role of Transcription Factor PU.I in the Activity of the Intronic Enhancer of the Eosinophil-Derived Neurotoxin (RNS2) Gene Blood, March 15, 1998; 91(6): 2126 - 2132. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Clarke, N. Arenzana, T. Hai, A. Minden, and R. Prywes Epidermal Growth Factor Induction of the c-jun Promoter by a Rac Pathway Mol. Cell. Biol., February 1, 1998; 18(2): 1065 - 1073. [Abstract] [Full Text]
|
|
|
|
 |
|
 C. Kitamura and M. Terashita Expressions of c-jun and jun-B Proto-oncogenes in Odontoblasts during Development of Bovine Tooth Germs Journal of Dental Research, April 1, 1997; 76(4): 822 - 830. [Abstract] [PDF]
|
|
|
|
 |
|
 D Pearce and K. Yamamoto Mineralocorticoid and glucocorticoid receptor activities distinguished by nonreceptor factors at a composite response element Science, February 19, 1993; 259(5098): 1161 - 1165. [Abstract] [PDF]
|
|