This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kayahara, M.
Right arrow Articles by Tournier, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kayahara, M.
Right arrow Articles by Tournier, C.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, May 2005, p. 3784-3792, Vol. 25, No. 9
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.9.3784-3792.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Selective Regulation of c-jun Gene Expression by Mitogen-Activated Protein Kinases via the 12-O-Tetradecanoylphorbol-13-Acetate- Responsive Element and Myocyte Enhancer Factor 2 Binding Sites

Midori Kayahara,{dagger} Xin Wang,{dagger} and Cathy Tournier*

Faculty of Life Sciences, University of Manchester, The Michael Smith Building, Oxford Road, Manchester M13 9PT, United Kingdom

Received 20 December 2004/ Accepted 26 January 2005

To further understand how the mitogen-activated protein kinase (MAPK) signaling pathways regulate AP-1 activity, we have elucidated the physiological role of these cascades in the regulation of c-jun gene expression. c-Jun is a crucial component of AP-1 complexes and has been shown in vitro to be a point of integration of numerous signals that can differentially affect its expression as well as its transcriptional activity. Our strategy was based on the use of (i) genetically modified fibroblasts deficient in components of the MAPK cascades and (ii) pharmacological reagents. The results demonstrate that c-Jun NH2-terminal protein kinase (JNK) is essential for a basal level of c-Jun expression and for c-Jun phosphorylation in response to stress. In addition to JNK, p38 MAPK or ERK1/2 and ERK5 are required for mediating UV radiation- or epidermal growth factor (EGF)-induced c-Jun expression, respectively. Further studies indicate that p38 MAPK inhibits the activation of JNK in response to EGF, causing a down-regulation of c-Jun. Overall, these data provide important insights into the mechanisms that ultimately determine the function of c-Jun as a regulator of cell fate.


* Corresponding author. Mailing address: Faculty of Life Sciences, University of Manchester, The Michael Smith Building, Oxford Road, Manchester M13 9PT, United Kingdom. Phone: 44 161 275 5417. Fax: 44 161 275 5082. E-mail: cathy.tournier{at}manchester.ac.uk.

{dagger} M.K. and X.W. contributed equally to this study.


Molecular and Cellular Biology, May 2005, p. 3784-3792, Vol. 25, No. 9
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.9.3784-3792.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Wang, X., Nadarajah, B., Robinson, A. C., McColl, B. W., Jin, J.-W., Dajas-Bailador, F., Boot-Handford, R. P., Tournier, C. (2007). Targeted Deletion of the Mitogen-Activated Protein Kinase Kinase 4 Gene in the Nervous System Causes Severe Brain Developmental Defects and Premature Death. Mol. Cell. Biol. 27: 7935-7946 [Abstract] [Full Text]  
  • Gross, N. D., Boyle, J. O., Du, B., Kekatpure, V. D., Lantowski, A., Thaler, H. T., Weksler, B. B., Subbaramaiah, K., Dannenberg, A. J. (2007). Inhibition of Jun NH2-Terminal Kinases Suppresses the Growth of Experimental Head and Neck Squamous Cell Carcinoma. Clin. Cancer Res. 13: 5910-5917 [Abstract] [Full Text]  
  • Wu, K., Liu, M., Li, A., Donninger, H., Rao, M., Jiao, X., Lisanti, M. P., Cvekl, A., Birrer, M., Pestell, R. G. (2007). Cell Fate Determination Factor DACH1 Inhibits c-Jun-induced Contact-independent Growth. Mol. Biol. Cell 18: 755-767 [Abstract] [Full Text]  
  • Adiseshaiah, P., Kalvakolanu, D. V., Reddy, S. P. (2006). A JNK-Independent Signaling Pathway Regulates TNF{alpha}-Stimulated, c-Jun-Driven FRA-1 Protooncogene Transcription in Pulmonary Epithelial Cells. J. Immunol. 177: 7193-7202 [Abstract] [Full Text]  
  • Spruill, L. S., McDermott, P. J. (2006). Regulation of c-jun mRNA expression in adult cardiocytes by MAP kinase interacting kinase-1 (MNK1). FASEB J. 20: 2133-2135 [Abstract] [Full Text]