This Article
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 Jaster, R.
Right arrow Articles by D'Andrea, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jaster, R.
Right arrow Articles by D'Andrea, A. D.

 Previous Article  |  Next Article 

Mol. Cell. Biol., Jun 1997, 3364-3372, Vol 17, No. 6
Copyright © 1997, American Society for Microbiology

JAK2 is required for induction of the murine DUB-1 gene

R Jaster, Y Zhu, M Pless, S Bhattacharya, B Mathey-Prevot and AD D'Andrea
Division of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

Cytokine receptors activate multiple signal transduction pathways, resulting in the induction of specific target genes. We have recently identified a hematopoietic cell-specific immediate-early gene, DUB-1, that encodes a growth-regulatory deubiquitinating enzyme. The DUB-1 gene contains a 112-bp enhancer element that is specifically induced by the beta c subunit of the interleukin-3 (IL-3) receptor. To investigate the mechanism of DUB-1 induction, we examined the effects of dominant- negative forms of JAK kinases, STAT transcription factors, and Raf-1 in transient transfection assays. In Ba/F3 cells, IL-3 induced a dose- dependent activation of DUB-1-luciferase (luc) and GAS-luc reporter constructs. A dominant-negative form of JAK2 (truncated at amino acid 829) inhibited the induction of DUB-1-luc and GAS-luc by IL-3. A dominant-negative form of STAT5 (truncated at amino acid 650) inhibited the induction of GAS-luc but not DUB-1-luc. A dominant-negative form of Raf-1 inhibited the induction of DUB-1-luc but had no effect on the induction of GAS-luc by IL-3. The requirement for JAK2 in the stimulation of the DUB-1 enhancer was further supported by the suppression of DUB-1 induction in Ba/F3 cells stably expressing the dominant-negative JAK2 polypeptide. We hypothesize that IL-3 activates a JAK2/Raf-1 signaling pathway that is required for DUB-1 induction and is independent of STAT5.


This article has been cited by other articles:

  • Schroder, K., Kohnen, A., Aicher, A., Liehn, E. A., Buchse, T., Stein, S., Weber, C., Dimmeler, S., Brandes, R. P. (2009). NADPH Oxidase Nox2 Is Required for Hypoxia-Induced Mobilization of Endothelial Progenitor Cells. Circ. Res. 105: 537-544 [Abstract] [Full Text]  
  • Ajjappala, B. S., Kim, Y.-S., Kim, M.-S., Lee, M.-Y., Lee, K.-Y., Ki, H.-Y., Cha, D.-H., Baek, K.-H. (2009). 14-3-3{gamma} Is Stimulated by IL-3 and Promotes Cell Proliferation. J. Immunol. 182: 1050-1060 [Abstract] [Full Text]  
  • Baek, K.-H., Kim, M.-S., Kim, Y.-S., Shin, J.-M., Choi, H.-K. (2004). DUB-1A, a Novel Deubiquitinating Enzyme Subfamily Member, Is Polyubiquitinated and Cytokine-inducible in B-lymphocytes. J. Biol. Chem. 279: 2368-2376 [Abstract] [Full Text]  
  • Lin, Y., Brown, L., Hedley, D. W., Barber, D. L., Benchimol, S. (2002). The death-promoting activity of p53 can be inhibited by distinct signaling pathways. Blood 100: 3990-4000 [Abstract] [Full Text]  
  • Baek, K.-H., Mondoux, M. A., Jaster, R., Fire-Levin, E., D'Andrea, A. D. (2001). DUB-2A, a new member of the DUB subfamily of hematopoietic deubiquitinating enzymes. Blood 98: 636-642 [Abstract] [Full Text]  
  • Barber, D. L., Beattie, B. K., Mason, J. M., Nguyen, M. H.-H., Yoakim, M., Neel, B. G., D'Andrea, A. D., Frank, D. A. (2001). A common epitope is shared by activated signal transducer and activator of transcription-5 (STAT5) and the phosphorylated erythropoietin receptor: implications for the docking model of STAT activation. Blood 97: 2230-2237 [Abstract] [Full Text]  
  • Sillaber, C., Gesbert, F., Frank, D. A., Sattler, M., Griffin, J. D. (2000). STAT5 activation contributes to growth and viability in Bcr/Abl-transformed cells. Blood 95: 2118-2125 [Abstract] [Full Text]  
  • Plowright, E. E., Li, Z., Bergsagel, P. L., Chesi, M., Barber, D. L., Branch, D. R., Hawley, R. G., Stewart, A. K. (2000). Ectopic expression of fibroblast growth factor receptor 3 promotes myeloma cell proliferation and prevents apoptosis. Blood 95: 992-998 [Abstract] [Full Text]  
  • Ilaria, R. L. Jr, Hawley, R. G., Van Etten, R. A. (1999). Dominant Negative Mutants Implicate STAT5 in Myeloid Cell Proliferation and Neutrophil Differentiation. Blood 93: 4154-4166 [Abstract] [Full Text]  
  • Ho, J. M.-Y., Beattie, B. K., Squire, J. A., Frank, D. A., Barber, D. L. (1999). Fusion of the ets Transcription Factor TEL to Jak2 Results in Constitutive Jak-Stat Signaling. Blood 93: 4354-4364 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»