◀ Back to FGF4
FGF4 — FGF8
Pathways - manually collected, often from reviews:
-
Reactome Reaction:
FGF4
→
FGF8
(reaction)
Carpenter et al., Exp Cell Res 1999, Hart et al., Mol Biol Cell 2001, Wong et al., Proc Natl Acad Sci U S A 2002, Lax et al., Mol Cell 2002, Fong et al., J Biol Chem 2003, Mohammadi et al., Nature 1992, Agazie et al., Oncogene 2003, Ibrahimi et al., Hum Mol Genet 2004, Furdui et al., Mol Cell 2006, Mohammadi et al., Mol Cell Biol 1991, Dionne et al., EMBO J 1990, Takeda et al., Clin Cancer Res 2007, Ahmed et al., Biochem J 2008, Byron et al., Cancer Res 2008, Schüller et al., Biochem J 2008, Qing et al., J Clin Invest 2009, Turner et al., Nat Rev Cancer 2010, Bai et al., Cancer Res 2010, Dutt et al., PloS one 2011, Wesche et al., Biochem J 2011, Klint et al., J Biol Chem 1995, Wang et al., Mol Cell Biol 1994, Mohammadi et al., Mol Cell Biol 1996, Ong et al., Biochem Biophys Res Commun 1996, Kanai et al., J Biol Chem 1997, Mohammadi et al., Science 1997, Kouhara et al., Cell 1997, Ong et al., Biochem Biophys Res Commun 1997, Hadari et al., Mol Cell Biol 1998, Raffioni et al., J Biol Chem 1998
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
Edom-Vovard et al., Dev Biol 2002
:
These results indicate that
Fgf4 expressed in muscle is
required for the maintenance of scleraxis and tenascin but not
Fgf8 expression in tendons
Liu et al., Development 2002
(Limb Deformities, Congenital) :
In this system,
FGF10 but not FGF8 protein injected into the mutant distal tip mesenchyme
restores Fgf8 expression in the AER
Saitsu et al., Mech Dev 2006
(Heart Defects, Congenital) :
Moreover, over-expression of
Fgf15 resulted in up-regulation of
Fgf8 expression in the isthmus/r1
Katayama et al., Int J Oncol 2010
(Prostatic Neoplasms) :
Overall, bicalutamide inhibits the cyclin A expression possibly by inhibiting
FGF-8 mRNA expression and FGF-8 protein secretion but not by
inhibiting FGF receptor ( FGFR ) signalling in androgen dependent cell lines, and by other mechanisms in androgen independent cell lines
Blagovic et al., PloS one 2011
:
Then we induce
FGF4 signaling in minimal chemically defined medium ( N2B27 ) and
inhibit FGF signaling in fully supplemented differentiation medium with cell secreted factors to determine that the non-FGF cell secreted factors are required to promote growth of differentiating mESCs
Haramis et al., Development 1995
:
Furthermore, no
Fgf-4 transcripts are
detected in the ld mutant AER, whereas
Fgf-8 transcripts remain expressed
Kettunen et al., Dev Dyn 1998
:
This data suggest
roles for
FGF-8 and FGF-9 during initiation of tooth development, and for
FGF-4 and FGF-9 during regulation of tooth shape