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

 Previous Article  |  Next Article 

Mol Cell Biol. 1992 October; 12(10): 4694-4705

Jun is phosphorylated by several protein kinases at the same sites that are modified in serum-stimulated fibroblasts.

Department of Molecular Oncology and Virology, Roche Institute of Molecular Biology, Nutley, New Jersey 07110.

ABSTRACT

c-jun is a member of the family of immediate-early genes whose expression is induced by factors such as serum stimulation, phorbol ester, and differentiation signals. Here we show that increased Jun synthesis after serum stimulation is accompanied by a concomitant increase in phosphorylation. Several serine-threonine kinases were evaluated for their ability to phosphorylate Jun in vitro. p34cdc2, protein kinase C, casein kinase II, and pp44mapk phosphorylated Jun efficiently, whereas cyclic AMP-dependent protein kinase and glycogen synthase kinase III did not. The sites phosphorylated by p34cdc2 were similar to those phosphorylated in vivo after serum induction. The major sites of phosphorylation were mapped to serines 63, 73, and 246. Phosphorylation of full-length Jun with several kinases did not affect the DNA-binding activity of Jun homodimers or Fos-Jun heterodimers. Comparison of the DNA binding and in vitro transcription properties of wild-type and mutated proteins containing either alanine or aspartic acid residues in place of Ser-63, -73, and -246 revealed only minor differences among homodimeric complexes and no differences among Fos-Jun heterodimers. Thus, phosphorylation of Jun did not produce a significant change in dimerization, DNA-binding, or in vitro transcription activity. The regulatory role of phosphorylation in the modulation of Jun function is likely to be considerably more complex than previously suggested.

This article has been cited by other articles:

• Manna, P. R, Stocco, D. M (2007). Crosstalk of CREB and Fos/Jun on a single cis-element: transcriptional repression of the steroidogenic acute regulatory protein gene. J Mol Endocrinol 39: 261-277 [Abstract] [Full Text]  
• Zhu, F., Choi, B. Y., Ma, W.-Y., Zhao, Z., Zhang, Y., Cho, Y. Y., Choi, H. S., Imamoto, A., Bode, A. M., Dong, Z. (2006). COOH-Terminal Src Kinase-Mediated c-Jun Phosphorylation Promotes c-Jun Degradation and Inhibits Cell Transformation. Cancer Res. 66: 5729-5736 [Abstract] [Full Text]  
• Cheng, C. K., Chow, B. K. C., Leung, P. C. K. (2003). An Activator Protein 1-Like Motif Mediates 17{beta}-Estradiol Repression of Gonadotropin-Releasing Hormone Receptor Promoter via an Estrogen Receptor {alpha}-Dependent Mechanism in Ovarian and Breast Cancer Cells. Mol. Endocrinol. 17: 2613-2629 [Abstract] [Full Text]  
• Edelstein, L. C., Lagos, L., Simmons, M., Tirumalai, H., Gelinas, C. (2003). NF-{kappa}B-Dependent Assembly of an Enhanceosome-Like Complex on the Promoter Region of Apoptosis Inhibitor Bfl-1/A1. Mol. Cell. Biol. 23: 2749-2761 [Abstract] [Full Text]  
• Laderoute, K. R., Calaoagan, J. M., Gustafson-Brown, C., Knapp, A. M., Li, G.-C., Mendonca, H. L., Ryan, H. E., Wang, Z., Johnson, R. S. (2002). The Response of c-Jun/AP-1 to Chronic Hypoxia Is Hypoxia-Inducible Factor 1{alpha} Dependent. Mol. Cell. Biol. 22: 2515-2523 [Abstract] [Full Text]  
• Wolfman, J. C., Palmby, T., Der, C. J., Wolfman, A. (2002). Cellular N-Ras Promotes Cell Survival by Downregulation of Jun N-Terminal Protein Kinase and p38. Mol. Cell. Biol. 22: 1589-1606 [Abstract] [Full Text]  
• Agazie, Y. M., Bagot, J. C., Trickey, E., Halenda, S. P., Wilden, P. A. (2001). Molecular mechanisms of ATP and insulin synergistic stimulation of coronary artery smooth muscle growth. Am. J. Physiol. Heart Circ. Physiol. 280: H795-H801 [Abstract] [Full Text]  
• Hu, X., Moscinski, L. C., Valkov, N. I., Fisher, A. B., Hill, B. J., Zuckerman, K. S. (2000). Prolonged Activation of the Mitogen-activated Protein Kinase Pathway Is Required for Macrophage-like Differentiation of a Human Myeloid Leukemic Cell Line. Cell Growth Differ. 11: 191-200 [Abstract] [Full Text]  
• Solis-Herruzo, J. A., Rippe, R. A., Schrum, L. W., de la Torre, P., Garcia, I., Jeffrey, J. J., Munoz-Yague, T., Brenner, D. A. (1999). Interleukin-6 Increases Rat Metalloproteinase-13 Gene Expression through Stimulation of Activator Protein 1 Transcription Factor in Cultured Fibroblasts. J. Biol. Chem. 274: 30919-30926 [Abstract] [Full Text]  
• Chen, D.-b., Westfall, S. D., Fong, H. W., Roberson, M. S., Davis, J. S. (1998). Prostaglandin F2{alpha} Stimulates the Raf/MEK1/Mitogen-Activated Protein Kinase Signaling Cascade in Bovine Luteal Cells. Endocrinology 139: 3876-3885 [Abstract] [Full Text]  
• Bird, T. A., Schooley, K., Dower, S. K., Hagen, H., Virca, G. D. (1997). Activation of Nuclear Transcription Factor NF-kappa B by Interleukin-1 Is Accompanied by Casein Kinase II-mediated Phosphorylation of the p65 Subunit. J. Biol. Chem. 272: 32606-32612 [Abstract] [Full Text]  
• Hakeda, Y., Shiokawa, M., Mano, H., Kameda, T., Raisz, L. G., Kumegawa, M. (1997). Prostaglandin F2{alpha} Stimulates Tyrosine Phosphorylation and Mitogen-Activated Protein Kinase in Osteoblastic MC3T3-E1 Cells via Protein Kinase C Activation. Endocrinology 138: 1821-1828 [Abstract] [Full Text]  
• Silberman, S., Janulis, M., Schultz, R. M. (1997). Characterization of Downstream Ras Signals That Induce Alternative Protease-dependent Invasive Phenotypes. J. Biol. Chem. 272: 5927-5935 [Abstract] [Full Text]  
• Yu, S.-M., Tsai, S.-Y., Guh, J.-H., Ko, F.-N., Teng, C.-M., Ou, J. T. (1996). Mechanism of Catecholamine-Induced Proliferation of Vascular Smooth Muscle Cells. Circulation 94: 547-554 [Abstract] [Full Text]  
• Weng, H., Choi, S.-Y., Faller, D. V. (1995). The Moloney Leukemia Retroviral Long Terminal Repeat trans-Activates AP-1-inducible Genes and AP-1 Transcription Factor Binding. J. Biol. Chem. 270: 13637-13644 [Abstract] [Full Text]  
• Watanabe, T., Waga, I., Honda, Z.-i., Kurokawa, K., Shimizu, T. (1995). Prostaglandin F[IMAGE]Stimulates Formation of p21-GTP Complex and Mitogen-activated Protein Kinase in NIH-3T3 Cells via G[IMAGE]-protein-coupled Pathway. J. Biol. Chem. 270: 8984-8990 [Abstract] [Full Text]  
• Chester, N., Yu, I. J., Marshak, D. R. (1995). Identification and Characterization of Protein Kinase CKII Isoforms in HeLa Cells. J. Biol. Chem. 270: 7501-7514 [Abstract] [Full Text]  
• Hibi, M, Lin, A, Smeal, T, Minden, A, Karin, M (1993). Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain.. Genes Dev. 7: 2135-2148 [Abstract]  
• Lange-Carter, C., Pleiman, C., Gardner, A., Blumer, K., Johnson, G. (1993). A divergence in the MAP kinase regulatory network defined by MEK kinase and Raf. Science 260: 315-319 [Abstract]