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FGF8 — SHH

Text-mined interactions from Literome

Power et al., Dev Dyn 1999 (Abnormalities, Multiple...) : Molecular analysis of RA-deficient limb buds revealed enhanced gli-3 and reduced hoxd-12, hoxd-13, shh , and fgf-4, while fgf-8 , en-1, and wnt-7a expression remained unaltered
Deutsch et al., Development 2001 : Cardiac mesoderm or FGF induces the local expression of sonic hedgehog , which in turn is inhibitory to pancreas but not to liver
Ohkubo et al., Neuroscience 2002 (Abnormalities, Drug-Induced...) : Similarly, loss of SHH expression in Shh mutant mice leads to increased BMP signaling and loss of Fgf8 expression in the prosencephalon
Aoto et al., Dev Biol 2002 : Whereas Fgf8 expression was almost absent in Shh-/- mutants, it was up-regulated in Gli3-/- ; Shh-/- double mutants, suggesting that SHH is not required for Fgf8 induction, and that GLI3 normally represses Fgf8 independently of SHH
Saitsu et al., Dev Dyn 2005 : In the previous genetic study, we showed that Shh is required for Fgf15 expression in the diencephalon and midbrain ... These findings indicate that Fgf15 is directly regulated by Shh signaling through Gli proteins
Esteve et al., Curr Opin Neurobiol 2006 : In addition, later on in development, Fgf controls the onset of retinal neurogenesis and Shh and GDF11 control its feedback regulation
Naruse et al., Dev Biol 2006 : However, FGF-2 did not induce dorsal expression of Shh , Patched1 or Nkx2.1, and co-injection of FGF-2 and a Shh inhibitor did not attenuate the induction of Olig2 and PDGFRalpha, suggesting that Shh signaling was not involved in this FGF-2 mediated dorsal induction
Fogarty et al., Proc Natl Acad Sci U S A 2007 (Neoplasms) : FGF also inhibits transcription of Shh target genes and prevents activation of a Gli-responsive promoter in fibroblasts, which suggests that it blocks Shh signaling upstream of Gli mediated transcription ... FGF mediated inhibition of Shh responses requires activation of FGF receptors and of ERK and JNK kinases, because it can be blocked by inhibitors of these enzymes
Hirashima et al., Bull Math Biol 2008 : A recent experimental observation suggests that the FGF-signal regulates the Shh expression in a feed-forward manner with activation and repression regulatory pathways
Vinothkumar et al., Dev Biol 2008 : Mutation of the binding sites or knockdown of Pea3 and Erm abolishes transgene expression, indicating that Fgf signaling regulates shh expression in the retina
Brito et al., Development 2008 : In our experimental design, the extra source of Shh activates Fgf8 , Bmp4 and Shh genes in caudal BA1 ectoderm in a spatial pattern similar to that of the oral epithelium, and regularly leads to the formation of two extra lower-jaw organizing centers with opposite rostrocaudal polarities
Prykhozhij et al., BMC developmental biology 2008 : The results presented here show that the role of Shh in this process is indirect, and is mediated by its effect on Fgf signaling
Lee et al., Dev Biol 2009 : Loss- and gain-of-function approaches indicate that Fgf signaling promotes shh expression in proximal epidermis, while Fgf/Ras signaling restricts shh expression from distal epidermis through induction of pea3 expression and maintenance of wnt5b
Mackem et al., Science signaling 2009 : Fibroblast growth factor ( FGF ) signaling from the epithelium regulates Sonic hedgehog (Shh) expression in the mesenchyme
Kobayashi et al., Dev Growth Differ 2010 : Shh induces Fgf8 expression in the ventral optic vesicle
Wang et al., Dev Biol 2010 : Lastly, we show that Shh/Gli2 signaling controls the diencephalic expression of Bone morphogenetic protein 4 (Bmp4) and Fibroblast growth factor 8 (Fgf8) , two genes that are known to play critical roles in patterning and growth of Rathke 's pouch
Mukhopadhyay et al., Dev Biol 2013 : Here FGF acutely suppressed Shh transcription within 90min but had significantly less effect on Eda, WNT, Notch or BMP pathways ... Furthermore, in vivo Fgfr2 loss-of-function in the ectoderm caused derepression of Shh, revealing a role for FGF in Shh regulation in the hair follicle
Grieshammer et al., Development 1996 : These observations support the hypothesis that Fgf8 is required for the induction of Shh expression during normal limb development
Logan et al., Development 1997 : Consistent with recent evidence that there is a reciprocal interaction between signalling molecules in the dorsal ectoderm, AER, and zone of polarising activity ( ZPA ), loss of Wnt7a, Fgf-8 and Fgf-4 expression leads to a decrease in expression of the signalling molecule Shh in the ZPA