Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol (January 15, 2003). doi:10.1152/ajpcell.00456.2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
284/5/C1262    most recent
00456.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Xu, H.
Right arrow Articles by Ghishan, F. K
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Xu, H.
Right arrow Articles by Ghishan, F. K
Submitted on September 30, 2002
Accepted on January 12, 2003

Transcriptional Regulation of the Human NaPi-IIb Cotransporter by EGF in Caco-2 Cells Involves c-Myb

Hua Xu1, Michael Inouye1, Eric Hines1, James F Collins1, and Fayez K Ghishan1*

1 Pediatrics, University of Arizona, Tucson, AZ, USA

* To whom correspondence should be addressed. E-mail: fghishan{at}peds.arizona.edu.

The type IIb sodium-phosphate (NaPi-IIb) cotransporter mediates intestinal phosphate absorption. Previous work in our laboratory has shown that EGF inhibited NaPi-IIb cotransporter expression through transcriptional regulation. To understand this regulation, progressively shorter hNaPi-IIb promoter constructs were used to define the EGF response region, and Gel Mobility Shift Assays (GMSAs) were used to characterize DNA-protein interactions. Promoter analysis determined that the EGF response region was located between -784 and -729 bp of the promoter. GMSAs and over-expression studies revealed an interaction between this promoter region and c-myb transcription factor. Inhibition of EGF receptor activation restored promoter function. Further studies suggested that MAPK, PKC and/or PKA pathways are involved in this regulation. In conclusion, these studies suggest that EGF decreases hNaPi-IIb gene expression by modifying the c-myb protein such that it inhibits transcriptional activation. We further conclude that this down-regulation of promoter function is mediated by EGF activated PKC/PKA and MAPK pathways. This is the first study that demonstrates the involvement of c-myb in regulation of intestinal nutrient absorption.




This article has been cited by other articles:


Home page
Am. J. Physiol. Cell Physiol.Home page
F. O'Mahony, F. Toumi, M. S. Mroz, G. Ferguson, and S. J. Keely
Induction of Na+/K+/2Cl- cotransporter expression mediates chronic potentiation of intestinal epithelial Cl- secretion by EGF
Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1362 - C1370.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
P. Hua, H. Xu, J. K. Uno, M. A. Lipko, J. Dong, P. R. Kiela, and F. K. Ghishan
Sp1 and Sp3 mediate NHE2 gene transcription in the intestinal epithelial cells
Am J Physiol Gastrointest Liver Physiol, July 1, 2007; 293(1): G146 - G153.
[Abstract] [Full Text] [PDF]


Home page
Exp PhysiolHome page
J. Marks, S. K. Srai, J. Biber, H. Murer, R. J. Unwin, and E. S. Debnam
Intestinal phosphate absorption and the effect of vitamin D: a comparison of rats with mice
Exp Physiol, May 1, 2006; 91(3): 531 - 537.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
H. Xu, J. K. Uno, M. Inouye, J. F. Collins, and F. K. Ghishan
NF1 transcriptional factor(s) is required for basal promoter activation of the human intestinal NaPi-IIb cotransporter gene
Am J Physiol Gastrointest Liver Physiol, February 1, 2005; 288(2): G175 - G181.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.