![]()
|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print August 10, 2004
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main D-60590
Corresponding Author: S.Frank{at}em.uni-frankfurt.de
Nitric oxide (NO) represents a short-lived mediator that pivotally drives keratinocyte movements during cutaneous wound healing. In this study, we have identified p68 DEAD box RNA helicase (p68) from a NO-induced differential keratinocyte cDNA library. Subsequently, we have analyzed regulation of p68 by wound-associated mediators in human and murine keratinocytes. NO, serum, growth factors and pro-inflammatory cytokines were potent inducers of p68 expression in the cells. p68 was constitutively expressed in the epithelial compartment of murine skin. Upon injury, we found a transient down-regulation of overall p68 protein in wound tissue. However, p68 did not completely disappear during early wound repair, as we found an expression of p68 protein in isolated wound margin tissue 24 h after wounding. Moreover, immunohistochemistry and cell fractionation analysis revealed a restricted localization of p68 in keratinocyte nuclei of the developing epithelium. Accordingly, also cultured keratinocytes showed a nuclear localization of the helicase. Moreover, confocal microscopy revealed a strong localization of p68 protein within the nucleoli of the cells. Functional analyses demonstrated that p68 strongly participates in keratinocyte proliferation and gene expression. Keratinocytes that constitutively overexpressed p68 protein were characterized by a marked increase in serum-induced proliferation and vascular endothelial growth factor (VEGF) expression, whereas down-regulation of endogenous p68 using small interfering RNA (siRNA) markedly attenuated serum-induced proliferation and VEGF expression. Altogether, our results suggest a tightly controlled expression and nucleolar localization of p68 in keratinocytes in vitro and during skin repair in vivo that functionally contributes to keratinocyte proliferation and gene expression.
J. Biol. Chem, 10.1074/jbc.M402467200
Submitted on March 4, 2004
Revised on June 25, 2004
Accepted on August 10, 2004
p68 dead box RNA helicase expression in keratinocytes: Regulation, nucleolar localization, and functional connection to proliferation and VEGF gene expression
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati What's this?
This article has been cited by other articles:
![]() |
C. Jalal, H. Uhlmann-Schiffler, and H. Stahl Redundant role of DEAD box proteins p68 (Ddx5) and p72/p82 (Ddx17) in ribosome biogenesis and cell proliferation Nucleic Acids Res., June 28, 2007; 35(11): 3590 - 3601. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Van Hoof, R. Passier, D. Ward-Van Oostwaard, M. W. H. Pinkse, A. J. R. Heck, C. L. Mummery, and J. Krijgsveld A Quest for Human and Mouse Embryonic Stem Cell-specific Proteins Mol. Cell. Proteomics, July 1, 2006; 5(7): 1261 - 1273. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. S. Haqqani, M. Nesic, E. Preston, E. Baumann, J. Kelly, and D. Stanimirovic Characterization of vascular protein expression patterns in cerebral ischemia/reperfusion using laser capture microdissection and ICAT-nanoLC-MS/MS FASEB J, November 1, 2005; 19(13): 1809 - 1821. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. P. Nittler, D. Hocking-Murray, C. K. Foo, and A. Sil Identification of Histoplasma capsulatum Transcripts Induced in Response to Reactive Nitrogen Species Mol. Biol. Cell, October 1, 2005; 16(10): 4792 - 4813. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |