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Am J Physiol Endocrinol Metab 283: E490-E495, 2002. First published May 7, 2002; doi:10.1152/ajpendo.00166.2002
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Vol. 283, Issue 3, E490-E495, September 2002

Fibroblast growth factor receptor 4 (FGFR4) mediates signaling to the prolactin but not the FGFR4 promoter

Shunjiang Yu1, Lei Zheng1, Sylvia L. Asa2, and Shereen Ezzat1

1 Department of Medicine, Mount Sinai Hospital and University of Toronto, 2 Department of Pathology, University Health Network and University of Toronto, The Freeman Centre for Endocrine Oncology, and The Ontario Cancer Institute, Toronto, Ontario, Canada M5G 2M9

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 prolactin (PRL) but not growth hormone 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 FGF-19-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.

fibroblast growth factor receptor 4; fibroblast growth factor-19; pituitary; Ikaros; Ets1


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