ライフサイエンスコーパス: FGF-7

1 s between HS and fibroblast growth factor-7 (FGF-7).

2 lated to keratinocyte growth factor (KGF, or FGF-7).

3 ty for mitogenic keratinocyte growth factor (FGF-7).

4 of the fibroblast growth factor (FGF) family FGF-7.

5 lycan in skin, is the principle cofactor for FGF-7.

6 n failed to exhibit the same properties with FGF-7.

7 module II resulted in a gain in affinity for FGF-7.

8 r high-affinity binding of FGF-1, FGF-2, and FGF-7.

9 a dual function chimera of FGF-7 and FGF-1 (FGF-7/1) which was resolved to 2.3 A.

10 ation of FGF-2 was an octasaccharide and for FGF-7 a decasaccharide.

11 vided by extract from lung mesenchyme, or by FGF-7, a growth factor also present in the early embryon

12 infiltrating Vgamma2Vdelta2 T cells produced FGF-7, a homeostatic mediator against tissue damages.

13 ion, we performed functional analysis of KGF/FGF-7 action.

14 In this report, we show that KGF/FGF-7 activated nuclear factor kappaB (NF-kappaB), which

15 thelial cell receptor, FGFR2IIIb, but unlike FGF-7 also binds the IIIb splice variant of FGFR1.

16 r elution from immobilized heparin than does FGF-7 and binds to four times the number of sites on the

17 eate the signaling pathways activated by KGF/FGF-7 and examine cellular response to KGF/FGF-7 stimula

18 the structure of a dual function chimera of FGF-7 and FGF-1 (FGF-7/1) which was resolved to 2.3 A.

19 to it conferred dual activities on both the FGF-7 and FGF-10 backbones.

20 hether this domain might underlie failure of FGF-7 and FGF-10 to bind to the FGFRIIIc isoforms.

21 Site-directed mutants of FGF-7 and FGF-10 were prepared to test whether this doma

22 FGFR2 ectodomain that abrogates response to FGF-7 and homologues from the stroma.

23 In the skin, both FGF-7 and mFGF-10 were expressed in the dermal, but not

24 FGF-7 receptor (FGFR2 IIIb) was treated with FGF-7 and with various glycosaminoglycans.

25 f mRNAs encoding Fibroblast Growth Factor-7 (FGF-7) and its high affinity receptor suggested that FGF

26 factor (FGF-1), keratinocyte growth factor (FGF-7), and FGF-10 are homologues with distinct specific

27 Differentiated myofibers express FGF-5, FGF-7, and reduced levels of FGF-6 mRNA.

28 on and suggest that paracrine sources of KGF/FGF-7 are one of the malignancy-contributing factors fro

29 eriments demonstrate that elevated levels of FGF-7 augment ureteric bud growth and increase the numbe

30 Although FGF-10 and FGF-7 bind and activate the same resident epithelial cel

31 of a papillary renal cell carcinoma, strong FGF-7 binding is seen.

32 bsolutely rejects FGF-7, resulted in gain of FGF-7 binding.

33 Stromal cell-derived FGF-7 binds and activates only the resident FGFR2IIIb in

34 wed that the soluble KGF receptor bound KGF (FGF-7) but not FGF-1 or FGF-2.

35 d those expressing the FGFR2IIIb/R1 chimera, FGF-7 caused a dose-dependent net inhibition of the popu

36 sessed in transgenic mice in which the human FGF-7 cDNA was controlled by a conditional promoter unde

37 -FGF), growth factors (TGF-beta, PDGF-A, and FGF-7), chemokines (MCP-1 and MIP-1alpha), and extracell

38 characterized the heparin-binding domain of FGF-7 defined by homology to that of FGF-1 and FGF-2 in

39 osaccharides capable of promoting FGF-2- and FGF-7-dependent cell proliferation.

40 Dermatan sulfate also enabled FGF-7-dependent phosphorylation of mitogen-activated pro

41 FGF-7 did not support cell proliferation in the absence

42 rneal epithelium in a novel Krt12-rtTA/tet-O-FGF-7 double transgenic mouse model in which cornea-spec

43 heparin enriched by affinity for immobilized FGF-7 exhibited anti-factor Xa activity similar to that

44 activates in vitro all FGFR subtypes, while FGF-7 exhibits absolute specificity for the IIIb splice

45 t prostate stromal cell-derived FGF-10, like FGF-7, exhibits the properties of an andromedin which ma

46 Induction of FGF-7 expression by doxycycline in the Ccsp-rtta x (Teto

47 ate a differential regulation of mFGF-10 and FGF-7 expression in vitro and during the wound healing p

48 n skin and most other tissue sites examined, FGF-7 fails to bind to basement membrane heparan sulfate

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

50 The canonical HBS in FGF-1, FGF-2, FGF-7, FGF-9, and FGF-18 differs in its size, and these

51 Here, we use a panel of FGFs (FGF-1, FGF-2, FGF-7, FGF-9, FGF-18, and FGF-21) spanning five FGF subf

52 structural basis to suggest that the unique FGF-7 heparin-binding (HB) domain underlies a specific r

53 We have recently identified a novel human FGF-7 homologue, named FGF-10.

54 R1 supports the binding of FGF-1, FGF-2, and FGF-7 in respective order of affinity.

55 localization, stability, and trafficking of FGF-7 in the microenvironment, and formation and activat

56 an effectively reconstituted the activity of FGF-7 in the perlecan-deficient cells.

57 blocked NF-kappaB activation, inhibited KGF/FGF-7-induced gene expression and cell migration and inv

58 ults demonstrate for the first time that KGF/FGF-7 induces NF-kappaB activation and that NF-kappaB pl

59 plays an essential role in regulation of KGF/FGF-7-inducible gene expression and KGF/FGF-7-initiated

60 KGF/FGF-7-inducible gene expression and KGF/FGF-7-initiated cellular responses.

61 FGF-7 is induced after injury and induces the proliferat

62 t members of the FGF family, the activity of FGF-7 is strongly influenced by binding to heparin, but

63 Keratinocyte growth factor (KGF or FGF-7) is a member of the heparin binding fibroblast gro

64 wth factor (KGF)/fibroblast growth factor-7 (FGF-7) is a paracrine- and epithelium-specific growth fa

65 st growth factor (FGF) family (also known as FGF-7), is an important protective factor for epithelial

66 nalysis suggests that FGF-10, in contrast to FGF-7, is a modest proliferation factor for the lung epi

67 blast growth factor (FGF)-10, a homologue of FGF-7, is expressed significantly in normal rat prostate

68 (IL)-1alpha, nerve growth factor (NGF), and FGF-7 (keratinocyte growth factor [KGF]) had no signific

69 Using biotinylated FGF-2 and FGF-7 (KGF) as probes, we have identified specific inter

70 llular acidification, whereas FGF-2 (basic), FGF-7 (KGF), TGF-beta1-beta3 and NGF had no significant

71 Collectively, these results demonstrate that FGF-7 levels modulate the extent of ureteric bud growth

72 In contrast to FGF-7, mFGF-10 expression was not induced during cutaneo

73 doxycycline in the Ccsp-rtta x (Teto)(7)-cmv-fgf-7 mice caused marked epithelial cell proliferation,

74 Taken together, Krt12-rtTA/tet-O-FGF-7 mice may be a suitable animal model for the study

75 cluded HSF2, NF-kappa B p65, ICE, IGF-II and FGF-7, MMP2, MMP14, and presenilin 2.

76 Further, this interplay between HS and FGF-7 modulated downstream ERK, AKT and p38 cascades, su

77 In this report, the levels of FGF-1, FGF-2, FGF-7 mRNA and their receptors FGFR-1 and FGFR-2, were i

78 Prenatally, doxycycline induced FGF-7 mRNA in respiratory epithelial cells in both Sp-c

79 uscle cells express FGF-1, FGF-2, FGF-6, and FGF-7 mRNA.

80 Neither FGF-7 nor FGF-10 will bind to IIIc isoforms of FGFR.

81 est this hypothesis we examined kidneys from FGF-7-null and wild-type mice.

82 , morphometric analyses indicate that mature FGF-7-null kidneys have 30+/-6% fewer nephrons than wild

83 ureteric bud and mature collecting system of FGF-7-null kidneys is markedly smaller than wild type.

84 ffects of excess fibroblast growth factor-7 (FGF-7) on both the proliferation and differentiation of

85 Effects of fibroblast growth factor-7 (FGF-7) on lung morphogenesis, respiratory epithelial cel

86 F-1 sequences into the C-terminal portion of FGF-7 or FGF-10 revealed that substitution of GSCKRG for

87 Fibroblast growth factor 7 (FGF-7) or keratinocyte growth factor (KGF), is a potent

88 nsgenic mouse model in which cornea-specific FGF-7 overexpression is achieved by doxycycline (Dox) tr

89 KGF/FGF-7 plays an essential role in the growth of epithelia

90 However, FGF-7 protein was detected in 70% (mean level=0.7 ng/ml)

91 lymphoid cell line (BaF/KGFR) containing the FGF-7 receptor (FGFR2 IIIb) was treated with FGF-7 and w

92 It acts exclusively through FGF-7 receptor (FGFR2/IIIb), which is expressed predomin

93 Similar to FGF-7, recombinant rat FGF-10 was a specific mitogen for

94 dings identify one signaling pathway for KGF/FGF-7-regulated cell migration and invasion and suggest

95 r, about the signaling pathways by which KGF/FGF-7 regulates the response of epithelial cells.

96 Protection of FGF-7 required interaction with specifically the fractio

97 an isoform that otherwise absolutely rejects FGF-7, resulted in gain of FGF-7 binding.

98 nd its high affinity receptor suggested that FGF-7 signaling may play a role in regulating ureteric b

99 Moreover, soluble FGF-7 specifically bound immobilized perlecan in a hepar

100 In addition, dermatan sulfate and FGF-7 stimulated growth of normal keratinocytes in cultu

101 and increased migration and invasion of KGF/FGF-7-stimulated human pancreatic ductal epithelial cell

102 F/FGF-7 and examine cellular response to KGF/FGF-7 stimulation, we performed functional analysis of K

103 Comparison of the FGF-7 structure to that of FGF-1 and FGF-2 revealed the

104 Here we report the structure of FGF-7 that has been solved to 3.1 A resolution by molecu

105 y RNase protection revealed that, similar to FGF-7, the expression of FGF-10 was responsive to androg

106 severely affected lines expressing FGF-4 or FGF-7, the lens epithelial cells exhibited a premature e

107 ncer, switching paracrine stimulation of KGF/FGF-7 to an autocrine loop.

108 a-strands 10 through 12 conferred ability on FGF-7 to bind to and activate FGFRIIIc without a signifi

109 kinase and promoted binding of radiolabeled FGF-7 to FGFR2 IIIb.

110 that FGF-10 binds with an affinity equal to FGF-7 to resident epithelial cell receptor, FGFR2IIIb, b

111 ice bearing both Ccsp-rtta and (Teto)(7)-cmv-fgf-7 transgenes survived, and lung morphology was norma

112 hy, and the activity to facilitate FGF-2 and FGF-7 was assayed by the cellular proliferation of cell

113 n contrast to FGF-1 and FGF-2, protection of FGF-7 was enhanced by heparin oligosaccharides of increa

114 Expression of FGF-7 was induced in respiratory epithelial cells of the

115 Epithelial cell hyperplasia caused by FGF-7 was largely resolved after removal of doxycycline.

116 Expression of FGF-7 was undetectable in non-transgenic epidermis, and

117 ion of human keratinocyte growth factor (KGF/FGF-7) was directed to hepatocytes during the later peri

118 In contrast to FGF-7 which is widely expressed among stromal cells in t

119 ch as fibroblast growth factor-2 (FGF-2) and FGF-7, which are present during the wound repair process

120 inetics, in both the absence and presence of FGF-7, which binds only the FGFR2IIIb ectodomain, were t

121 receptor 2 that binds the ligands FGF-1 and FGF-7 with high affinity, and is expressed exclusively b