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1 and repressed by fibroblast growth factor-8 (FGF-8).
2 chymal cells are equicompetent to respond to Fgf-8.
3 However, very little is known about human FGF-8.
9 y loop between the fibroblast growth factors FGF-8 and FGF-10 plays a key role in limb initiation and
10 ceptor blocking antibodies, we now show that FGF-8 and FGF-17 target OL progenitors, inhibiting their
12 of polarising activity (ZPA), loss of Wnt7a, Fgf-8 and Fgf-4 expression leads to a decrease in expres
16 sion of the fibroblast growth factor-8 gene (Fgf-8) appears as normal in the ectoderm over the prospe
17 eveloping face and the limb buds we identify Fgf-8 as the likely candidate signalling molecule that r
18 Fgf-4, expression, whereas the expression of Fgf-8, as at earlier stages, is initially unaffected.
21 , continuous and widespread misexpression of FGF-8 causes limb truncations and skeletal alterations w
22 port that Xenopus embryos expressing ectopic FGF-8 develop an abundance of ectopic neurons that exten
23 morpholino oligonucleotide-mediated loss of FGF-8 expression in vivo substantially reduced the pheno
31 that in the mandibular arch, as in the limb, Fgf-8 functions in combination with CD44, a cell surface
34 poral and spatial expression patterns of the FGF-8 gene suggest its involvement in gastrulation, regi
35 st growth factor (bFGF), Sonic hedgehog, and FGF-8 in a serum-free N-2 culture medium to foster diffe
36 s and cell fates are fixed and maintained by Fgf-8 in conjunction with another epithelial signal, end
37 Finally, we also show that the induction of Fgf-8 in the limb ectoderm by FGF-10 is mediated by the
41 report here that another FGF family member, FGF-8 is able to protect rat hippocampal cultures from o
44 istent with the hypothesis that the multiple FGF-8 isoforms are functionally redundant and function t
48 pression patterns and the specificity of the FGF-8 isoforms for known fibroblast growth factor (FGF)
50 stic molecular interactions between Activin, FGF-8, Lefty-1, Nodal, BMPs and Car that cooperate to co
51 tumors in Wnt-1 transgenic mice and because FGF-8 manifested its autocrine mitogenic activity in SC-
52 , it is possible that aberrant expression of FGF-8 may be present in human cancers which are hormone
56 explants is unaffected by the expression of FGF-8 or a dominant-negative Ras (N17ras), suggesting th
57 patterning influences of sonic hedgehog and FGF-8 or the more generic process of neuronal differenti
61 In explant cultures, neutralizing Ab for FGF-8 rescued development of the myocardial calcium tran
62 d fail to express sonic hedgehog, FGF-4, and FGF-8, signaling molecules that have been implicated in
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