ライフサイエンスコーパス: FGF-4

1 t) which encodes fibroblast growth factor-4 (FGF-4).

2 or autocrine action of its secreted protein, FGF-4.

3 % in GH3 cells in the presence or absence of FGF-4.

4 AER is mediated in part by the production of FGF-4.

5 stem (ES) cells, which are unable to produce FGF-4.

6 ssing FGF-8, FGF-9 and some lines expressing FGF-4.

7 GF-4+/+ ES cells when they are cultured with FGF-4.

8 FGF-4 (0.1-50 ng/ml) caused a dose-dependent 2.5-fold in

9 In vertebrates, Fgf 4, 8, 9, and 17 are all expressed in the AER.

10 Fibroblast growth factor-4 (FGF-4), a highly mitogenic protein encoded by the k-fgf/

11 FGF-4 microcarrier beads we have found that FGF-4 acts as a potent and specific chemoattractive agen

12 ave shown that early mouse embryos with both FGF-4 alleles inactivated are developmentally arrested s

13 Thus, ES cells with both FGF-4 alleles inactivated should shed light on the impor

14 n and characterization of ES cells with both FGF-4 alleles inactivated.

15 FGF-4 also induces Shh.

16 tuitary tumor cell cultures with recombinant FGF-4 and also stably transfected pituitary cell lines w

17 activates the expression of HoxD13, HoxD11, Fgf-4 and BMP-2 ectopically, consistent with cFHF-2 play

18 se, and rat MAPCs, cultured on Matrigel with FGF-4 and HGF, differentiated into epithelioid cells tha

19 uggests that BMP-2 is involved in regulating Fgf-4 and HoxD gene expression in the normal limb bud.

20 FGF-4 and SDF-1 enhanced vascular cell adhesion molecule

21 Both FGF-4 and SHH induce local expression of Bmp-4, while BM

22 To address this, FGF-2 and FGF-4, and extracellular domain constructs of FR1-IIIc (

23 FGF-3, FGF-4, and FGF-8 were not detectable by RT-PCR in either

24 elements and fail to express sonic hedgehog, FGF-4, and FGF-8, signaling molecules that have been imp

25 is initiated by a continuous stripe of Shh, Fgf-4, and Ptc expression in the epithelium, which then

26 The primary effect of FGF-4 appeared to be on the stromal cells of the long-te

27 The cell migration response to FGF-4 appears to be independent of the known inductive a

28 Beads soaked in FGF-1, FGF-2 and FGF-4 are able to induce additional limbs when applied t

29 ns of the AER signalling molecules Fgf-8 and Fgf-4 are altered.

30 Hoxd-13 and Fgf-4 are initially expressed posteriorly until about th

31 n of the FIN genes is induced in response to FGF-4 as well as to serum in NIH3T3 cells with delayed k

32 duction of differentiation in PC-12 cells by FGF-4 (as well as by NGF) did not result in significant

33 versely, BMP-2 or BMP-4, in combination with FGF-4, can readily induce cardiac myocyte formation in p

34 ared with vector controls, overexpression of FGF-4 clearly induced expansion of cushion mesenchyme to

35 the expression of the stem cell marker gene FGF-4 decreases.

36 SDF-1 and FGF-4 diminished thrombocytopenia after myelosuppression

37 Thus, FGF-4 does not appear to act as an autocrine growth fact

38 cell lineage and elaboration of Hoxd-13 and Fgf-4 domains.

39 To understand the roles of FGF-4 during early development, we prepared genetically

40 examined the effects of exogenous FGF-1 and FGF-4 during lens regeneration.

41 se cells and elucidate the role of FGF-2 and FGF-4 during normal development and in the pathogenesis

42 should shed light on the important roles of FGF-4 during the early stages of mammalian development a

43 mammalian development and help determine why FGF-4-/- embryos die shortly after implantation.

44 FGF-1, FGF-2, and FGF-4 enhanced mitogen-activated protein kinase (MAPK) a

45 e HMG and POU cis-regulatory elements of the FGF-4 enhancer are dependent on one another and function

46 re physically associated with the endogenous FGF-4 enhancer but weakly associated with the endogenous

47 d Oct-3, which bind to adjacent sites on the FGF-4 enhancer DNA and synergistically activate transcri

48 in domains occurs in a cooperative manner on FGF-4 enhancer DNA, and the loss of this cooperative int

49 arrangement of the binding sites within the FGF-4 enhancer DNA.

50 Previous studies have shown that FGF-4 enhancer function is mediated by at least three cr

51 present evidence that p300 mediation of the FGF-4 enhancer requires acetyltransferase activity.

52 tify a second essential HMG motif within the FGF-4 enhancer that binds the transcription factor Sox-2

53 plays an important role in the action of the FGF-4 enhancer.

54 imulate the FGF-4 promoter when bound to the FGF-4 enhancer.

55 ic interaction between Oct-3 and Sox2 on the FGF-4 enhancer.

56 es with FGF-4 production as determined by an FGF-4 enzyme-linked immunosorbent assay, an increase in

57 y formed in vitro from FGF-4-/- ES cells and FGF-4+/+ ES cells when they are cultured with FGF-4.

58 differentiated progeny formed in vitro from FGF-4-/- ES cells and FGF-4+/+ ES cells when they are cu

59 In addition, we demonstrate that the FGF-4-/- ES cells can differentiate in vitro after expos

60 The FGF-4-/- ES cells do not require FGF-4 to proliferate in

61 ber of differentiated cells derived from the FGF-4-/- ES cells, in particular cells with many of the

62 We also demonstrate that FGF-4-/- ES cells, like their unmodified counterparts, a

63 Whereas FGF-2 binds HS ubiquitously, FGF-4 exhibits a restricted pattern, failing to bind HS

64 In addition, the two signals can activate Fgf-4 expression in anterior ridge and HoxD expression i

65 rimordium is associated with an extension of Fgf-4 expression in the epithelium and bifurcation of Me

66 ing activity (ZPA), loss of Wnt7a, Fgf-8 and Fgf-4 expression leads to a decrease in expression of th

67 chick limb bud and the induction of Shh and Fgf-4 expression.

68 0-23) similarly down-regulates Shh, and also Fgf-4, expression, whereas the expression of Fgf-8, as a

69 transgenic mice that express different FGFs (FGF-4, FGF-7, FGF-8, FGF-9) specifically in the lens.

70 Together, these results suggest a role of FGF-4 for cardiac valve leaflet formation through prolif

71 The FGF-4 gene is regulated during early development by a po

72 The FGF-4 gene was truncated by DNA rearrangement with a nov

73 itro are affected by the inactivation of the FGF-4 gene, in particular specific cells that form durin

74 scription, we examined the regulation of the FGF-4 gene.

75 r and are required for the activation of the FGF-4 gene.

76 role in mediating enhancer activation of the FGF-4 gene.

77 isolation of the fibroblast growth factor 4 (FGF-4) gene by NIH3T3 transformation assay using DNA fro

78 scription of the fibroblast growth factor-4 (FGF-4) gene during early development is controlled by a

79 ously shown that fibroblast growth factor 4 (FGF-4) gene expression in embryonal carcinoma cells requ

80 promoter of the fibroblast growth factor-4 (FGF-4) gene is strongly activated by B-Myb in HeLa cells

81 H4 hst-transfected cells strongly expressing FGF-4 grew more aggressively as assessed by histologic i

82 s, while untreated subcultures, made without FGF-4, grew erratically and generally lost the capacity

83 Subcultures made in the presence of FGF-4 had up to 10-fold increases in plating efficiency

84 IGF-I, insulin, FGF-2 and FGF-4 have been implicated in the reciprocal interaction

85 Additionally, whereas FR2c binds all FGF-4-HS complexes, FR1c fails to bind FGF-4-HS in most

86 s all FGF-4-HS complexes, FR1c fails to bind FGF-4-HS in most tissues, as well as in Raji-S1 cells ex

87 To further test the proliferative effect of FGF-4 in cardiac cushion expansion in vivo (ovo), FGF-4

88 While overexpression of FGF-4 in the MCF-7 breast carcinoma cell line confers th

89 We have found that FGF-4, in addition to FGF-2, is a mitogen for NPCs isola

90 insulin, and, to a lesser extent, FGF-2 and FGF-4 induce the proliferation and directed outgrowth of

91 ort that IGF-I and insulin, but not FGF-2 or FGF-4, induce the formation of limb bud-like structures

92 -precardiac mesoderm with combined BMP-2 and FGF-4 induced cardiogenesis in the majority of explants,

93 The response to FGF-4 is dose dependent in both the number of cells stim

94 on of whose corresponding RNAs is induced by FGF-4 (K-FGF) in murine NIH3T3 fibroblasts.

95 I cell labeling with ectopic implantation of FGF-4 microcarrier beads we have found that FGF-4 acts a

96 ificant increase in proliferative ability in FGF-4 microinjected cardiac cushion mesenchyme as compar

97 dependent of the known inductive activity of FGF-4 on Shh gene expression.

98 ole of the apical ectodermal ridge (AER) and FGF-4 on the control of cell migration during limb bud m

99 In less severely affected lines expressing FGF-4 or FGF-7, the lens epithelial cells exhibited a pr

100 , activated ras, fibroblast growth factor-4 (FGF-4), or epidermal growth factor receptor (EGFR) media

101 Despite the lack of Shh, FGF-4, or BMP-2 expression, the hoxd genes are expressed

102 hown that fibroblast growth factor (FGF)-1-, FGF-4-, or vascular endothelial growth factor (VEGF/VPF)

103 ps in the following order: BMP-2, BMP-4, and FGF-4 (peptide growth factors); Wnt 7a and Shh (Drosophi

104 her primordia that are more strongly Shh and Fgf-4 positive.

105 These findings suggest that BMP-2 and FGF-4 possess respective differentiative and proliferati

106 rom infection with the virus correlates with FGF-4 production as determined by an FGF-4 enzyme-linked

107 ts were screened for hst mRNA expression and FGF-4 production.

108 ains of B-Myb required for activation of the FGF-4 promoter were identified.

109 Gal4/p300 fusion proteins can stimulate the FGF-4 promoter when bound to the FGF-4 enhancer.

110 nd p300, inhibits enhancer activation of the FGF-4 promoter.

111 eraction between the distal enhancer and the FGF-4 promoter.

112 er but weakly associated with the endogenous FGF-4 promoter.

113 n and elongation into prevalvular structure, FGF-4 protein was added to the cushion mesenchymal cells

114 in cardiac cushion expansion in vivo (ovo), FGF-4 protein was microinjected into stage 18 chick inne

115 In addition, Shh and FGF-4 reciprocally reinforce each other's expression via

116 The expression of Shh and Fgf-4 remains dependent upon the continued synthesis of

117 or-1 (SDF-1) and fibroblast growth factor-4 (FGF-4), restored thrombopoiesis in Thpo(-/-) and Mpl(-/-

118 This suggests that FGF-4 seeks a specific HS sulfation pattern, distinct fr

119 Whereas FGF-4 supports cardiogenesis in precardiac mesoderm, it

120 or postimplantation development, addition of FGF-4 to blastocyst outgrowths increased the number of e

121 Addition of FGF-4 to human long-term bone marrow cultures increased

122 The FGF-4-/- ES cells do not require FGF-4 to proliferate in vitro, and addition of FGF-4 to

123 Importantly, addition of FGF-4 to the culture medium dramatically increases the n

124 F-4 to proliferate in vitro, and addition of FGF-4 to the medium has little or no effect on their gro

125 A bioassay that measures the potency of the FGF-4 transgene carried by a replication incompetent ade

126 acy-indicating assay, demonstrating that the FGF-4 transgene product carried by Ad5FGF-4 is biologica

127 liferative ability was strongly suggested in FGF-4-treated mesenchymal cells as judged by the incorpo

128 FGF-1 or FGF-4 treatment in lentectomized eyes resulted in the in

129 FGF-4 treatment of wild-type GH4 cells, transiently tran

130 FGF-1, FGF-2, or FGF-4 was added directly to the culture medium or was re

131 vector, and found that ectopic expression of Fgf-4 was induced in the anterior part of the apical ect

132 2 for binding to FGFR-1 and FGFR-1L, whereas FGF-4 was less efficient.

133 S) from the Kaposi fibroblast growth factor (FGF-4) were used to transduce enzymatically active Cre p

134 ion in contrast with the activators, SHH and FGF-4, which induce feather formation.

135 a replication-defective retrovirus encoding FGF-4 with the reporter, bacterial beta-galactosidase wa

136 formed 3T3 cells that constitutively produce FGF-4 with their normal counterpart.