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Am J Physiol Endocrinol Metab (May 7, 2002). doi:10.1152/ajpendo.00166.2002
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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.




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