ライフサイエンスコーパス: FGF-1

1 ndary HBS, ranging from none (FGF-9) to two (FGF-1).

2 (numbering scheme of the 140-residue form of FGF-1).

3 after addition of fibroblast growth factor (FGF-1).

4 which is, at least in part, mediated through FGF-1.

5 izing at each cysteine position in wild-type FGF-1.

6 ation, cysteine to serine mutations in human FGF-1.

7 sine phosphorylation of cortactin induced by FGF-1.

8 ontaining TATA and CAAT consensus sequences (FGF-1.

9 ion of DNA synthesis of endothelial cells by FGF-1.

10 oid arthritis synovium express receptors for FGF-1.

11 o a phenylalanine at this position in bovine FGF-1.

12 enhanced by the combination of anti-CD3 and FGF-1.

13 ed that four of the synthetic sugars bind to FGF-1.

14 important determinant for the expression of FGF-1.

15 nding protein was involved in the release of FGF-1.

16 f truncated FGF-1 but not to the full-length FGF-1.

17 of human IgG1 (Fc) at the amino terminus of FGF-1.

18 steps of nuclear translocation mechanism of FGF-1.

19 or to initiate DNA synthesis in response to FGF-1.

20 eparin-binding protein that co-purified with FGF-1.

21 GFR3 IIIb-expressing cells responded only to FGF-1.

22 leading to the formation of the homodimer of FGF-1.

23 matory cytokines in cord slices treated with FGF-1.

24 ion of ERK1/2 induced by HRGbeta1 but not by FGF-1.

25 ined the compartmental localization of 99mTc-FGF-1.

26 iation rate constants spanning over 20-fold (FGF-1, 2,900,000 M(-1) s(-1) and FGF-9, 130,000 M(-1) s(

27 lpha(2)M* bind specifically and saturably to FGF-1, -2, -4, and -6, although the binding to alpha(2)M

28 several members of the FGF family including FGF-1, -2, -4, and -6, while FGFR3 IIIb-expressing cells

29 MM14 cells express FGF-1, -2, -6, and -7 and produce FGF protein, yet they

30 mmunoblot analysis confirmed the presence of FGF-1, -2, and -7 and TGFbeta-1, -2, and -3 in condition

31 itro collagen gel assay, we show that serum, FGF-1, -2, and -7, VEGF, and EGF stimulate epicardial EM

32 upport a model in which myocardially derived FGF-1, -2, or -7 promotes epicardial EMT, while TGFbeta-

33 Blocking antisera directed against FGF-1, -2, or -7 substantially inhibit conditioned mediu

34 AG3 imaging, and subsequently, 99mTc-labeled FGF-1 (99mTc-FGF-1) was imaged after i.v. injection.

35 re of human acidic fibroblast growth factor (FGF-1) a combination of five mutations were accommodated

36 er CpG site in the 5'-flanking region of the Fgf-1.A isoform was also methylated specifically by Dnmt

37 se heart is the most abundant source for the FGF-1.A mRNA.

38 termined the transcription start site of the FGF-1.A mRNA.

39 ents in embryonic myocytes and, furthermore, FGF-1 achieves its effects on different K+ currents via

40 K,S and IK,I was unaffected, indicating that FGF-1 achieves its regulatory effects on electrical deve

41 ctodermal origin; in addition, expression of FGF-1 (acidic FGF) is increased at several sites of chro

42 becular meshwork cell proliferation; and (c) FGF-1 (acidic), TGF-alpha, EGF, IL-1alpha, IL-1beta, HGF

43 GF-2) stimulated cell proliferation, whereas FGF-1 (acidic), transforming growth factor (TGF) alpha,

44 In contrast, an FGF-1 affinity matrix enriched the fraction of crude hep

45 FGF-1 alone induces modest nuclear translocation of kapp

46 nologic injury, and recent studies show that FGF-1 also may interact with cells of the immune system.

47 Fibroblast growth factor 1 (FGF-1, also known as acidic FGF) is a mitogen for a vari

48 scripts encoding fibroblast growth factor 1 (FGF-1, also known as aFGF) have been previously identifi

49 se in Etd(+) uptake by astrocytes induced by FGF-1, although they are activated by FGF-1 treatment.

50 For the present studies, we focused on FGF-1 and -2 and investigated interactions with recombin

51 , for the glycosaminoglycan-binding proteins FGF-1 and BACE, and for the heterotypic adhesion molecul

52 unoprecipitation of the receptor bound to Fc-FGF-1 and by flow cytometry showing binding of fusion pr

53 ta show that mitogenic pathways activated by FGF-1 and EGF are regulated by c-Src protein levels and

54 AMX binds to FGF-1 and enhances its conformational stability.

55 R cells), express high levels of full-length FGF-1 and exhibit a complete spectrum of transformed phe

56 rected mutagenesis, exchanging residues from FGF-1 and FGF-2 and correlating structural changes with

57 We conclude that FGF-BP1 binds directly to FGF-1 and FGF-2 and positively modulates the biological

58 arin hexasaccharide that cocrystallized with FGF-1 and FGF-2 and protected both against protease in s

59 Both FGF-1 and FGF-2 are expressed by developing muscle cells

60 Previously, it has been noted that FGF-1 and FGF-2 can oligomerize in the presence of HLGAG

61 FGF-1 and FGF-2 competed efficiently with (125)I-FGF-2 f

62 show here that, under identical conditions, FGF-1 and FGF-2 differ in the degree and kind of oligome

63 FGF-1 and FGF-2 differ in their ability to bind isoforms

64 lexes of heparin and recombinant FGFR4 bound FGF-1 and FGF-2 equally.

65 cells binds only FGF-1, whereas FGFR1 binds FGF-1 and FGF-2 equally.

66 In summary, FGF-1 and FGF-2 exert opposite effects on voltage-depend

67 resident FGFR2IIIb in epithelial cells while FGF-1 and FGF-2 exhibit a broader interaction with multi

68 main of FGF-7 defined by homology to that of FGF-1 and FGF-2 in complexes with heparin.

69 ht to be coordinated at least in part by the FGF-1 and FGF-2 members of the fibroblast growth factor

70 Therefore, we investigated whether FGF-1 and FGF-2 oligomerize by the same mechanism or by

71 opment by FGFs is a complex process in which FGF-1 and FGF-2 play distinct roles.

72 We also found that FGF-1 and FGF-2 promote proliferation, migration, and su

73 Comparison of the FGF-7 structure to that of FGF-1 and FGF-2 revealed the strongly conserved Calpha b

74 Surprisingly, even though FGF-1 and FGF-2 share more than 80% sequence similarity

75 Furthermore, an extensive analysis of FGF-1 and FGF-2 uncomplexed and HLGAG complexed crystal

76 for FGF-1 and supported the binding of both FGF-1 and FGF-2 when complexed with FGFR1.

77 These findings indicate that FGFR-1L binds FGF-1 and FGF-2 with high affinity and is capable of mit

78 nds and activates fibroblast growth factors (FGF-1 and FGF-2) and induces angiogenesis in some human

79 Taken together, these data show that FGF-1 and FGF-2, despite their sequence homology, differ

80 e fibroblast growth factor (FGF) prototypes, FGF-1 and FGF-2, lack a signal sequence, but both contai

81 In contrast to FGF-1 and FGF-2, protection of FGF-7 was enhanced by hep

82 complex with FGFR that discriminates between FGF-1 and FGF-2.

83 radiolabeled heparin bound independently to FGF-1 and FGF-2.

84 Since FGF-1 and FGF-3 can both activate one FGF receptor isofo

85 nction, we examined the effects of exogenous FGF-1 and FGF-4 during lens regeneration.

86 ant of FGF receptor 2 that binds the ligands FGF-1 and FGF-7 with high affinity, and is expressed exc

87 FGF-1 and HRGbeta1 also reduced the inhibition of ERK1/2

88 f-1 by all three of the growth factors, both FGF-1 and HRGbeta1, unlike EGF, induced a prolonged acti

89 the FGF-1 receptor, PD173074, inhibits both FGF-1 and injury-induced release.

90 In this paper, we describe expression of FGF-1 and its receptors, FGFR-2 (KGFR and bek variants)

91 rain a purified fraction that contained both FGF-1 and p40 Syn-1 and report that the brain-derived FG

92 to repress the heat shock-induced release of FGF-1 and p40 Syn-1 in a concentration-dependent manner,

93 d the effects of amlexanox on the release of FGF-1 and p40 Syn-1 in response to stress in vitro.

94 S100A13 may be involved in the regulation of FGF-1 and p40 Syn-1 release in response to temperature s

95 e between the monomer and homodimer forms of FGF-1 and resolution by conventional and limited denatur

96 The restricted pattern of FGF-1 and RPTPrho implies that these molecules may have

97 exes with FGFR4 restored the specificity for FGF-1 and supported the binding of both FGF-1 and FGF-2

98 noblot analysis, it was possible to identify FGF-1 and Syn-1 as potential components of a denaturant-

99 Effects of acidic fibroblast growth factor (FGF-1) and basic fibroblast growth factor (FGF-2) were t

100 c cytokine, acidic fibroblast growth factor (FGF-1) and its high-affinity receptors, in both relevant

101 or both the third and fourth cassettes from FGF-1, and neither exhibited any affinity for fibrinogen

102 Furthermore, FGF-BP1 enhances FGF-1- and FGF-2-dependent proliferation of NIH-3T3 fibr

103 Thus, activation of FGF-1- and HRGbeta1-specific signaling causes MEK-depend

104 A serum-free culture containing SCF, TPO, FGF-1, angiopoietin-like 5, and IGFBP2 supports an appro

105 In the latter, FGF-1 application promotes the activation of microglia a

106 FGF-1 applied to rat spinal astrocytes in culture initia

107 ted conditions but that paracrine effects of FGF-1 are also involved in the enhancement of tumor grow

108 Such stabilized mutations of FGF-1 are shown to exhibit significant increases in effe

109 he adjacent N and C terminus beta-strands of FGF-1 are shown to provide a substantial increase in sta

110 Amplification of FGF-1 at 5q31 in ovarian cancer tissues leads to increas

111 teine mutation was introduced into wild-type FGF-1 at adjacent position Ala66, which is known to part

112 Among them, FGF-1.B is the major transcript expressed specifically i

113 glioblastoma cells resulted in repression of FGF-1.B promoter activity.

114 c fibroblast growth factor (FGF)-1 promoter (FGF-1.B) binds multiple nuclear factors, and this bindin

115 RR1 and RR2) in the brain-specific promoter, FGF-1.B.

116 synaptotagmin-1, neither synaptotagmin-1 nor FGF-1:beta-gal are able to access the stress-induced rel

117 r kinetics and pharmacological properties as FGF-1:beta-gal.

118 caffold protein IB1(JIP-1b) [9, 10], nor can FGF-1 bind to IB2.

119 In the presence of heparin, FGF-1 binds and activates in vitro all FGFR subtypes, wh

120 The position of the RPTPrho and FGF-1 boundary on the rostrocaudal axis of the cerebella

121 nd to the mitogenic stimulation of truncated FGF-1 but not to the full-length FGF-1.

122 eparin potentiates the mitogenic activity of FGF-1 by increasing the affinity for its receptor and by

123 In addition, the human FGF-1 C131S mutant showed a decrease in homodimer format

124 In some human T cells, FGF-1 can induce signals necessary for production of int

125 Application of FGF-1 causes a similar release of ATP in the uninjured s

126 (1) In cultures of spinal astrocytes FGF-1 causes the release of ATP, and ATP causes opening

127 X-2(-/-) mice following in vivo injection of FGF-1 compared with either COX-1(-/-) or wild-type mice.

128 FGF-1 contains three cysteine residues, two of which are

129 Further, replacement of the FGF-1 cytosol retention domain with the corresponding do

130 its inability to repress the function of the FGF-1 cytosol retention domain.

131 tween residues 83 and 154 is responsible for FGF-1 cytosol retention in NIH 3T3 cells.

132 We prepared a series of FGF-1 deletion mutants fused to the reporter gene, beta-

133 Early studies with FGF-1 demonstrated its presence in bovine brain as a nov

134 ubcellular distribution of exogenously added FGF-1 demonstrated that full-length FGF-1 fails to trans

135 -1 PTB resulted in a significant decrease of FGF-1-dependent tyrosine phosphorylation of endogenous S

136 the phenylalanine to tyrosine in the bovine FGF-1 did not reduce the ability of the iodinated protei

137 FGF-1 did not significantly alter sensory epithelial cel

138 g-term exposure of the embryonic myocytes to FGF-1 downregulated inward rectifier K+ current (IK(IR))

139 ot able to direct the nuclear association of FGF-1 due to its inability to repress the function of th

140 tyrosine phosphorylation of Snt (or Frs2), a FGF-1 early signaling protein that links to Ras.

141 in vivo SIGNIFICANCE STATEMENT: We find that FGF-1 elevates [Ca(2+)]i in spinal astrocytes, which cau

142 sgenic mice expressing in the lens a form of FGF-1 engineered to be secreted show premature different

143 teins were constructed from human and bovine FGF-1 expression constructs and tested for their heparin

144 at multiple levels, and the significance of FGF-1 expression in human breast tumors is uncertain.

145 he possibility that the paracrine effects of FGF-1 expression may allow the partial agonist propertie

146 Morphological analysis further reveals that FGF-1 fails to induce the formation of polarized lamelli

147 ly added FGF-1 demonstrated that full-length FGF-1 fails to translocate to the nuclei of NR31 cells.

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

149 FGF-1, FGF-2, and FGF-4 enhanced mitogen-activated prote

150 g module II of FGFR1 supports the binding of FGF-1, FGF-2, and FGF-7 in respective order of affinity.

151 are dispensable for high-affinity binding of FGF-1, FGF-2, and FGF-7.

152 Significantly increased expression of FGF-1, FGF-2, and PDGF-B was noted in the allografts at

153 pacities of the aged myocardial GAGs to bind FGF-1, FGF-2, and VEGF but not HB EGF.

154 The canonical HBS in FGF-1, FGF-2, FGF-7, FGF-9, and FGF-18 differs in its si

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

156 Common activation of STAT pathways by FGF-1, FGF-2, IGF-1, or PDGFaa and their synergistic act

157 prove useful as "second generation" forms of FGF-1 for application in angiogenic therapy.

158 oliferation, they are impaired to respond to FGF-1 for the shape change and cell migration.

159 why FGF-2 forms sequential oligomers whereas FGF-1 forms only dimers.

160 Acidic fibroblast growth factor (FGF-1) functions as a potent hormonal inducer of wound r

161 The Fc-FGF-1 fusion protein retained FGF function as determined

162 f the G isoform of fibroblast growth factor (Fgf-1.G) on mouse chromosome 18.

163 der to elucidate the regulatory mechanism of FGF-1 gene expression, the mouse promoter containing TAT

164 s indicate that certain CpG sites within the Fgf-1 gene locus are preferentially methylated by Dnmt3a

165 the entire transcriptional unit of the mouse FGF-1 gene, including four promoters, is characterized.

166 a might regulate fibroblast growth factor 1 (FGF-1) gene expression which was previously implemented

167 Because FGF-1 has a similar structure to FGF-2 but does not bind

168 For example, the low Tm of FGF-1 has been postulated to play an important role in t

169 The nonclassical export of FGF-1 has been shown to be inhibited by an anti-allergic

170 However, certain mutants of FGF-1 have been described that exhibit a significant inc

171 te thermodynamic parameters of unfolding for FGF-1 have been unavailable, presumably due to effects o

172 Fibroblast growth factors (FGFs), such as FGF-1, have been shown to induce differentiation of lens

173 FGF-2 and that this binding is inhibited by FGF-1, heparan sulfate, and heparinoids.

174 cells caused by fibroblast growth factor 1 (FGF-1), heregulin beta1 (HRGbeta1), and epidermal growth

175 100A13 is important for the formation of the FGF-1 homodimer and the subsequent secretion of the sign

176 X-induced inhibition of the formation of the FGF-1 homodimer is observed both under cell-free conditi

177 a free cysteine at position 66 destabilizes FGF-1; however, upon oxidation, a near-optimal disulfide

178 corresponding sites in the third cassette of FGF-1 imparted high-affinity binding with apparent disso

179 In addition, the involvement of FGF-1 in a number of pathophysiological conditions, incl

180 n harbors a single tyrosine residue in human FGF-1 in contrast to a phenylalanine at this position in

181 We have utilized signal transduction by FGF-1 in PC12 cells to compare the ability of FGFR-1 and

182 ow describe in vivo imaging and targeting of FGF-1 in renal transplanted rats.

183 ntisense-Syn-1 gene represses the release of FGF-1 in response to heat shock.

184 To understand the action of FGF-1 in T cells, studies were initiated in Jurkat T cel

185 Reduced renal binding of 99mTc-FGF-1 in the allogeneic transplanted kidney was consiste

186 We also showed increased expression of FGF-1 in the CNS of ts1-infected mice.

187 vesicular domain of Syn-1 is associated with FGF-1 in the extracellular compartment of FGF-1-transfec

188 Unique glomerular targeting of 99mTc-FGF-1 in the transplanted kidney provides additional evi

189 r 2 (IGF-2), and fibroblast growth factor-1 (FGF-1) in serum-free medium.

190 ss fibroblast growth factor (FGF) prototype, FGF-1, in vitro as a stress-induced pathway in which FGF

191 ng showed that the heparin-binding domain of FGF-1 includes cysteine-131 and that cysteine-131, upon

192 We conclude that autocrine effects of FGF-1 increase the ability of MCF-7 breast cancer cells

193 downstream signaling components and abrogate FGF-1-induced antiestrogen-resistant growth.

194 FGF-1-induced dye uptake by astrocytes is prevented by B

195 ras in the pre-B lymphoid cell line BaF3 for FGF-1-induced mitogenesis revealed that the JM region di

196 rosine phosphorylation of cortactin, and the FGF-1-induced redistribution of cortactin and F-actin we

197 t from the CD28 costimulation pathway, since FGF-1-induced Rel/kappaB binding proteins do not contain

198 Fibroblast growth factor 1 (FGF-1) induces neurite outgrowth in PC12 cells.

199 The FGF-1 initiated cascade may play an important role in sp

200 FGF-1 is abundantly expressed in the synovium in rheumat

201 FGF-1 is an example of a protein that is regulated, in p

202 These data suggest the following: (i) FGF-1 is associated with Syn-1 and S100A13 in vivo; (ii)

203 l exocytotic pathway and that the release of FGF-1 is dependent on synaptotagmin-1.

204 the anti-inflammatory compound amlexanox and FGF-1 is involved in inflammation, we examined the effec

205 utations, the results indicate that although FGF-1 is known for generally poor thermal stability, the

206 ion of MAP kinase in response to full-length FGF-1 is not sufficient for mitogenesis.

207 We show here that the growth factor FGF-1 is proinflammatory in the spinal cord and explore

208 n vitro as a stress-induced pathway in which FGF-1 is released as a latent homodimer with the p40 ext

209 Since FGF-1 is released in response to heat shock as a mitogen

210 iary structure, the resulting mutant form of FGF-1 is substantially more stable.

211 heparin-binding affinity the mutant form of FGF-1 is surprisingly approximately 70 times more potent

212 FGF-1 is the prototypical member of the FGF family, and

213 These results show that position 83 in FGF-1 is thermodynamically optimized to accept a free cy

214 Furthermore, FGF-1 is unable to induce tyrosine phosphorylation of co

215 Fibroblast growth factor 1 (FGF-1) is a potent chemotactic factor and induces tyrosi

216 Human acidic fibroblast growth factor (FGF-1) is a potent mitogen and angiogenic factor, with r

217 Human acidic fibroblast growth factor (FGF-1) is a powerful mitogen and angiogenic factor with

218 il protein human fibroblast growth factor-1 (FGF-1) is made up of a six-stranded antiparallel beta-ba

219 Acidic fibroblast growth factor (FGF-1), keratinocyte growth factor (FGF-7), and FGF-10 a

220 Fibroblast growth factor (FGF-1) lacks a signal sequence and is exported by an unc

221 These data indicate that FGF-1 may be able to utilize the cytosolic face of conve

222 vel approach for the design of drugs against FGF-1-mediated disorders.

223 ssion levels (P = .021 and < .001), and both FGF-1 mRNA and protein levels were significantly associa

224 FGF-1 mRNA copy number was significantly correlated with

225 Acidic fibroblast growth factor (FGF-1) mRNA follows a similar cerebellar expression patt

226 from synaptotagmin-1 is able to utilize the FGF-1 non-classical exocytotic pathway and that the rele

227 ice, indicating that the mitogenic effect of FGF-1 on the breast tumor cells was important in the est

228 FGF-1 or -2 and heparin promoted the fibroblast phenotyp

229 latelet-derived growth factor (PDGF)-aa, and FGF-1 or -2 in the lens.

230 l signal sequence for secretion not found in FGF-1 or -2.

231 blasts replated and grown in the presence of FGF-1 or FGF-2 (20 ng/ml) plus heparin (5 microg/ml) in

232 elia and failed to potentiate the effects of FGF-1 or FGF-2.

233 luble KGF receptor bound KGF (FGF-7) but not FGF-1 or FGF-2.

234 FGF-1 or FGF-4 treatment in lentectomized eyes resulted

235 A serum-free medium containing SCF, TPO, and FGF-1 or Flt3-L cannot significantly support expansion o

236 We found that either FGF-1 or HRGbeta1 but not EGF substantially reduced the

237 expression inhibited the acquired ability of FGF-1-overexpressing cells to form colonies in soft agar

238 ession severely inhibited the ability of the FGF-1-overexpressing cells to form tumors without estrog

239 observed in the pulmonary vein implied that FGF-1-overexpressing MCF-7 cells are deficient in their

240 p40 Syn-1 and report that the brain-derived FGF-1:p40 Syn-1 aggregate is associated with the calcium

241 ntly, there is an increasing need to monitor FGF-1 pharmacokinetics and distribution for both therape

242 Increased angiogenesis resulting from FGF-1 production by the transfected cells with a concomi

243 ence has no significant effect on either the FGF-1 promoter or E47 promoter.

244 onstrated the exaggerated appearance of both FGF-1 protein and mRNA in resident inflammatory and tubu

245 udies showed significant correlation between FGF-1 protein expression and CD31+ staining in the tumor

246 This functional Fc-FGF-1 protein should prove useful in identifying FGFR-ex

247 ible for the lost heparin affinity, chimeric FGF-1 proteins were constructed from human and bovine FG

248 injured spinal cord, and an inhibitor of the FGF-1 receptor, PD173074, inhibits both FGF-1 and injury

249 To determine the biologic relevance of the FGF-1 release pathway in vivo, we sought to resolve and

250 o temperature stress in vitro; and (iii) the FGF-1 release pathway may be accessible to pharmacologic

251 this group, a significant reduction in 99mTc-FGF-1 renal binding was measured by imaging analyses, as

252 sine phosphorylation of cortactin induced by FGF-1 requires the tyrosine residues 421, 482 and 466, w

253 postnatal weeks two and six, for RPTPrho and FGF-1, respectively.

254 The frequency of FGF-1-responsive T cells is increased in the peripheral

255 cubation of the NR cells with either form of FGF-1 resulted in its binding to cell-surface FGF recept

256 We demonstrate that transient exposure to FGF-1 results in a significant decrease in Fos transcrip

257 In contrast, bovine FGF-1 retained its heparin affinity even after iodinatio

258 y screening with fibroblast growth factor-1 (FGF-1) revealed that four of the synthetic sugars bind t

259 o heparin even after iodination while bovine FGF-1 (S131C) lost its binding affinity to heparin upon

260 Mutating this tyrosine residue in the human FGF-1 sequence to phenylalanine did not restore the hepa

261 fferent substitutions of shorter segments of FGF-1 sequences into the C-terminal portion of FGF-7 or

262 Constructions with substitution of FGF-1 sequences spanning the entire C-terminus encoded i

263 99mTc-FGF-1 serves as a new radiotracer to measure in vivo tar

264 and endothelial cells treated with exogenous FGF-1 showed a significant increase in cell motility and

265 a are the first to show a connection between FGF-1 signaling and NF-kappaB activation outside of embr

266 Our findings suggest that the FGF-1 signaling pathway may be responsible for the overe

267 Exogenous FGF-1 stimulated expression of OPN mRNA and protein in R

268 -conditioned medium inhibited both basal and FGF-1-stimulated AF migration.

269 tein (MAP) kinases, respectively, attenuated FGF-1-stimulated OPN mRNA expression.

270 These experiments show that FGF-1 stimulation of Jurkat T cells provides a second si

271 tin and F-actin were unaffected by transient FGF-1 stimulation.

272 In contrast, a mutant human FGF-1 that has cysteine-131 replaced with serine (C131S)

273 Mutant forms of FGF-1 that substitute a serine residue at these cysteine

274 Consistent with the mitogenic response to FGF-1, the lack of Src does not affect the tyrosine phos

275 ut interfering with their ability to produce FGF-1, thereby allowing possible paracrine effects to st

276 helial HSPG was deficient for the binding of FGF-1 to both FGFR complexes.

277 transplanted rats showed a redistribution of FGF-1 to the glomerular compartment.

278 FGF-1 transfectants formed large, vascularized tumors in

279 tribute to an increased malignant phenotype, FGF-1-transfected MCF-7 cells were retransfected with a

280 th FGF-1 in the extracellular compartment of FGF-1-transfected NIH 3T3 cells following temperature st

281 i.v. injection of FGF-1-transfected tumor cells produced no pulmonary macr

282 se spinal cord slices ex vivo, we found that FGF-1 treatment for 1 h increases the percentage of GFAP

283 FGF-1 treatment of RASMCs enhanced RASMC-conditioned med

284 ced by FGF-1, although they are activated by FGF-1 treatment.

285 unfolding (DeltaH, DeltaG, and DeltaCp) for FGF-1 using differential scanning calorimetry (DSC).

286 e inhibitory action of AMX on the release of FGF-1, using a variety of biophysical techniques includi

287 iptions of the electrostatic interactions of FGF-1 vs FGF-2 with cation exchangers were obtained, and

288 OPN mRNA induction by FGF-1 was attenuated by PD 166866, a highly selective an

289 OPN mRNA induction by FGF-1 was completely inhibited by either actinomycin D o

290 Although the full-length FGF-1 was detected in the nuclear fractions of both NIH/

291 This response to FGF-1 was not observed in astrocytes in slices of cerebr

292 The regulation of IK(IR) by FGF-1 was prevented by the cytoplasmic tyrosine kinase i

293 s showed that the C-terminal region of human FGF-1 was responsible for the loss of heparin affinity.

294 and subsequently, 99mTc-labeled FGF-1 (99mTc-FGF-1) was imaged after i.v. injection.

295 the 5q31 region, fibroblast growth factor 1 (FGF-1) was selected for further validation study.

296 role of the free cysteine at position 83 in FGF-1, we constructed Ala, Ser, Thr, Val, and Ile mutati

297 FGFR4) in liver parenchymal cells binds only FGF-1, whereas FGFR1 binds FGF-1 and FGF-2 equally.

298 a translationally related oligomer, whereas FGF-1, which does not have this interface, forms only a

299 To better characterize the interaction of FGF-1 with FGF receptors on T cells, a fusion protein wa

300 During the course of labeling human FGF-1 with Na(125)I and chloramine T, it was observed th