AJP - Endo Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab (May 7, 2002). doi:10.1152/ajpendo.00166.2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/3/E490    most recent
00166.2002v1
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 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 Yu, S.
Right arrow Articles by Ezzat, S.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Yu, S.
Right arrow Articles by Ezzat, S.

Articles in PresS, published online ahead of print May 7, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00166.2002
Submitted on April 19, 2002
Accepted on May 4, 2002

Fibroblast Growth Factor Receptor 4 (FGFR4) Mediates Signalling to the Prolactin but Not FGFR4 Promoter

ShunJiang Yu1, Lei Zheng1, Sylvia L. Asa2*, and Shereen Ezzat1

1 Medicine, University of Toronto, Toronto, ON, Canada; Medicine, Mount Sinai Hospital, Toronto, ON, Canada
2 Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Pathology, University Health Network, Toronto, ON, Canada

* To whom correspondence should be addressed. E-mail: sylvia.asa{at}uhn.on.ca.

Fibroblast growth factor receptors (FGFRs) have been implicated in a multitude of activities. Signaling of the 23 members of the FGF family is mediated through FGFR1-4. We show that FGF-19, which selectively binds FGFR4, can induce PRL but not GH expression. FGF-19 also stimulated MAPK activation, an effect that was abrogated by a soluble dominant negative (dn) form of FGFR4. The response of the pituitary PRL promoter to FGF maps to an Ets-Pit1 binding site. We have previously shown that the hematopoietic zinc finger-containing transcription factor Ikaros (Ik) regulates FGFR4 as part of an overlapping site with that for an Ets-type factor in the FGFR4 promoter. Thus, we examined whether FGF-19 might regulate its own receptor through the Ets-Ik element in the FGFR4 promoter. Ets stimulated and dn-Ets inhibited basal FGFR4 and PRL promoter activity. In contrast, Ets enhanced FGF19-induced PRL activation but failed to confer an effect for FGF-19 on the FGFR4 promoter. We conclude that FGFR4 mediates FGF-19 signaling to the PRL promoter. Our data also suggest a possible functional role for Ik in sorting Ets signals to the FGFR4 promoter as distinct from the PRL promoter where Ets partners with Pit1.




This article has been cited by other articles:


Home page
 Cancer Res.Home page
S. Loeper, S. L. Asa, and S. Ezzat
Ikaros Modulates Cholesterol Uptake: A Link between Tumor Suppression and Differentiation
Cancer Res., May 15, 2008; 68(10): 3715 - 3723.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
S. Ezzat, P. Huang, A. Dackiw, and S. L. Asa
Dual Inhibition of RET and FGFR4 Restrains Medullary Thyroid Cancer Cell Growth
Clin. Cancer Res., February 1, 2005; 11(3): 1336 - 1341.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2002 by the American Physiological Society.