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

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

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

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

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

14 FGF-4 also induces Shh.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 0-23) similarly down-regulates Shh, and also Fgf-4, expression, whereas the expression of Fgf-8, as a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 2 for binding to FGFR-1 and FGFR-1L, whereas FGF-4 was less efficient.

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

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

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

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