ライフサイエンスコーパス: IGFBP-1

1 hich could be corrected by pretreatment with IGFBP-1.

2 owth in transgenic mice overexpressing human IGFBP-1.

3 higher than that of nonphosphorylated human IGFBP-1.

4 an IGFBP-1, whereas it can phosphorylate rat IGFBP-1.

5 mTOR and CSNK-2beta but not between mTOR and IGFBP-1.

6 ivity, they were numerously positive for the IGFBP-1.

7 corticoid-induced transcription of PEPCK and IGFBP-1.

8 in vitro, but it did not phosphorylate human IGFBP-1.

9 ion could be inhibited with excess unlabeled IGFBP-1.

10 (exposed to [32P]H3PO4) secrete 32P-labeled IGFBP-1.

11 dues immediately preceding it, interact with IGFBP-1.

12 e features of these molecules that recognize IGFBP-1.

13 to polymerization by Tg compared with native IGFBP-1.

14 extent compared with native (phosphorylated) IGFBP-1.

15 produce IGFBP-2, -3, -4, -5, and -6 but not IGFBP-1.

16 the IGFBP-5 N-domain that are not present in IGFBP-1.

17 IGFBP-1, -2, -4, and -5 were of intermediate effectivene

18 125I-IGFBP-3, -4, and -5 but not 125I-IGFBP-1, -2, and -6 bound to TbetaR-V as demonstrated by

19 IGF binding protein-1 (IGFBP-1), a hepatocyte-derived secreted protein, is requ

20 nsulin-like growth factor binding protein 1 (IGFBP-1), a secreted protein that may modulate the activ

21 ding protein of IGFBP-1 which modifies IGF-I/IGFBP-1 actions resulting in enhanced IGF effects.

22 IGFBP-1 acts via beta1-integrin and focal-adhesion-kinas

23 ed IGFBP-1 from human plasma and from (125)I-IGFBP-1.alpha(2)M complexes formed in vitro.

24 The (125)I-IGFBP-1/alpha(2)M association could be inhibited with ex

25 ever, in addition to inhibiting IGF effects, IGFBP-1 also diminished basal motility.

26 We assayed circulating IGFBP-1 among 144 pancreatic cancer cases that occurred

27 , plasma protein and hepatic mRNA content of IGFBP-1, an inhibitor of IGF bioactivity, was elevated i

28 g transactivation activity, whereas those of IGFBP-1 and -6 had no activity.

29 We used recombinant IGFBP-1 and a synthetic RGD-containing hexapeptide in co

30 ights into the transcriptional regulation of IGFBP-1 and contribute to our understanding of the role

31 nt showed markedly amplified PLA signals for IGFBP-1 and CSNK-2beta (approximately 18-fold, P = 0.000

32 otential perinuclear co-localization between IGFBP-1 and CSNK-2beta and a nuclear co-localization bet

33 tion assay (PLA) indicated proximity between IGFBP-1 and CSNK-2beta as well as mTOR and CSNK-2beta bu

34 l rendering of the PLA images validated that IGFBP-1 and CSNK-2beta interactions were in the perinucl

35 ween circulating concentrations of IGF-I and IGFBP-1 and development of glucose tolerance.

36 suggest that IGF-I and its binding proteins IGFBP-1 and IGFBP-2 have potentially beneficial effects

37 n of each IGF-I amino acid side chain toward IGFBP-1 and IGFBP-3, combining alanine-scanning mutagene

38 to IGF-1 specifically and blocks binding of IGFBP-1 and IGFBP-3.

39 diabetes, we examined the impact of this on IGFBP-1 and its phosphorylation status in diabetic pregn

40 in obese mice to investigate the effects of IGFBP-1 and its RGD domain on insulin sensitivity, insul

41 which results in elevated levels in serum of IGFBP-1 and limits the biological availability of IGFs r

42 ining C/EBPbeta interacts with IRSs from the IGFBP-1 and PEPCK genes in a sequence-specific fashion a

43 ific effects of insulin on the expression of IGFBP-1 and perhaps multiple hepatic genes through a con

44 Roles of IGFBP-1 and platelet factor 4 in HC.HA antiangiogenic ac

45 d not contain PEDF and TSP-1 but did contain IGFBP-1 and platelet factor 4 while significantly suppre

46 libraries have yielded a peptide that binds IGFBP-1 and produces IGF-like activity at sub-micromolar

47 rences in the phosphorylation state of human IGFBP-1 and rat IGFBP-1 in these transgenic mice.

48 ssociates with the phosphorylated isoform of IGFBP-1 and that when complexed to alpha(2)M, IGFBP-1 ca

49 ve a high affinity and specificity for human IGFBP-1 and to inhibit IGF-I binding.

50 es (ir) of the IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta),

51 nsulin-like growth factor binding protein-1 (IGFBP-1) and phosphoenolpyruvate carboxykinase (PEPCK).

52 nsulin-like growth factor binding protein 1 (IGFBP-1), and insulin-like growth factor binding protein

53 like growth factor binding protein-1 and -3 (IGFBP-1, and -3), growth hormone, insulin, and cytokines

54 e measured serum concentrations of IGF-I and IGFBP-1, and assessed the relation between these peptide

55 transgenic mouse, which overexpresses human IGFBP-1, and explored the effect of this protein on meta

56 e phosphoenolpyruvate carboxykinase (PEPCK), IGFBP-1, and G6Pase promoters.

57 eated monkeys had SF levels of IGF-1, IGF-2, IGFBP-1, and IGFBP-3 that were intermediate between the

58 IGFBP-3 and elevated vegetable protein with IGFBP-1-and, to our knowledge, is novel in reporting the

59 igate whether prediagnostic plasma levels of IGFBP-1 are associated with pancreatic cancer risk, we d

60 Circulating insulin and IGFBP-1 are potential mediators of the association betwe

61 nsulin-like growth factor binding protein 1 (IGFBP-1) are associated with insulin resistance and pred

62 ms of IGFBP-1 may increase the usefulness of IGFBP-1 as a predictor of fetal growth in both normal an

63 Random Forest modeling identified fS-p-IGFBP-1 as one of the top five predictors of liver fat (

64 e report interactions between CSNK-2beta and IGFBP-1 as well as mTOR and CSNK-2beta, providing strong

65 sustained dysregulation of the insulin/IGF-I/IGFBP-1 axis is associated with impaired glucose toleran

66 The insulin/IGF binding protein-1 (IGFBP-1) axis is important in coordinating insulin- and

67 The influence of low plasma IGFBP-1 became progressively stronger with time; among c

68 n-helix peptide motif that are necessary for IGFBP-1 binding and structural integrity.

69 tations, E3A and F49A, selectively decreased IGFBP-1 binding by 34- and 100-fold, whereas IGFBP-3 aff

70 nsulin-like growth factor-binding protein-1 (IGFBP-1) binds to insulin-like growth factors (IGFs) and

71 ed insulin inhibition of basal expression of IGFBP-1 but not PEPCK.

72 stic Muller cells did not detect message for IGFBP-1, but revealed progressive increases in message a

73 d increased the level of the IGF-I inhibitor IGFBP-1 by 11-fold.

74 IGFBP-1 can affect cellular functions independently of I

75 GFBP-1 and that when complexed to alpha(2)M, IGFBP-1 can still bind IGF-I.

76 Overexpression of IGFBP-1 caused growth and developmental retardation unde

77 ne if, after incubation of bp1-01 with IGF-I.IGFBP-1 complexes, anabolic and insulin-like effects of

78 ch leads to release of free IGF-I from IGF-I.IGFBP-1 complexes.

79 that for every decrease of 2.73 microg/l in IGFBP-1 concentration, there was a 43% increase in the o

80 IGFBP-1 concentrations increased with age in Pakistanis

81 were relatively insulinopenic but had higher IGFBP-1 concentrations.

82 Because IGFBP-1 contains a RGD motif important in binding of fib

83 IGFBP-1 contributes to glucose counterregulation, and ob

84 e physiological context, we used a human (h) IGFBP-1 cosmid clone so that transgene expression is res

85 t circulating IGF-I and its interaction with IGFBP-1 could be important determinants of glucose homoe

86 Moreover, IGFBP-1 could have dual effects on cancer cell motility

87 To determine whether IGFBP-1 could prevent liver injury that entails direct s

88 factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) could be important determinants of glucose homo

89 r localization and potential interactions of IGFBP-1, CSNK-2beta, and mTOR as a prerequisite for prot

90 increased with rHGH treatment, whereas serum IGFBP-1 decreased compared with placebo (p < .05).

91 IGFBP-1 deficiency was associated with massive hepatocyt

92 IGFBP-1-deficient livers had enhanced signaling via the

93 ta1, a hepatocyte apoptogen, was observed in IGFBP-1-deficient livers that correlated with the appear

94 The effect of IGFBP-1 depends on its phosphorylation status; phosphory

95 addition of higher concentrations of native IGFBP-1 did inhibit the protein synthesis response, and

96 Maternal decidual IGFBP-1 excess is also associated with impaired fetal gr

97 sis, we have studied the effects of decidual IGFBP-1 excess on fetoplacental growth in transgenic mic

98 We therefore hypothesized that IGFBP-1 exerts potentially beneficial effects, either di

99 sion or CoCl2 treatment resulted in elevated IGFBP-1 expression in zebra fish embryos.

100 The induction of IGFBP-1 expression may be a conserved physiological mech

101 These results show that RTEF-1-stimulated IGFBP-1 expression may be central to the mechanism by wh

102 y embryogenesis and mediates hypoxia-induced IGFBP-1 expression.

103 native IGFBP-1 multimers, however, Q66A/Q67A IGFBP-1 failed to polymerize.

104 owed that the affinity of phosphorylated rat IGFBP-1 for IGF-1 was 3.9-fold higher than that of nonph

105 tion with pure tissue transglutaminase (Tg), IGFBP-1 formed covalently linked multimers that were sta

106 i-alpha(2)M antibodies co-immunoprecipitated IGFBP-1 from human plasma and from (125)I-IGFBP-1.alpha(

107 this phenomenon, we purified phosphorylated IGFBP-1 from normal human plasma by immunoaffinity chrom

108 tional significance since alpha(2)M protects IGFBP-1 from proteolysis and abrogates the inhibitory ef

109 measurement of fasting serum phosphorylated IGFBP-1 (fS-pIGFBP-1) helps to predict liver fat compare

110 These findings indicate that IGFBP-1 functions as a critical hepatic survival factor

111 lates IGFBP-1 in the human fetus in vivo and IGFBP-1 gene expression and protein in vitro.

112 suggest that HIF-1 mediates hypoxia-induced IGFBP-1 gene expression in early development by selectiv

113 ecular mechanisms underlying hypoxia-induced IGFBP-1 gene expression in the embryonic tissues are not

114 a-inducible factor 1 in hypoxia induction of IGFBP-1 gene expression.

115 nes containing large regions 5' of the mouse IGFBP-1 gene sequence were isolated, subcloned, and sequ

116 tion, mice with a targeted disruption of the IGFBP-1 gene were generated.

117 induced transcription of either the PEPCK or IGFBP-1 gene.

118 r and more distal regulatory elements of the IGFBP-1 gene.

119 nsulin-like growth factor-binding protein-1 (IGFBP-1) gene and that a C/EBP-binding site can mediate

120 nsulin-like growth factor binding protein 1 (IGFBP-1) gene by means of an insulin-responsive element

121 nsulin-like growth factor binding protein 1 (IGFBP-1) gene is dramatically altered by changes in the

122 nsulin-like growth factor binding protein-1 (IGFBP-1) gene is highly expressed in fetal, perinatal, a

123 nsulin-like growth factor-binding protein-1 (IGFBP-1) genes bind members of the FKHR and HNF3 subclas

124 eas those in the top quartile of circulating IGFBP-1 had a significant reduction in mortality (HR = 0

125 cells were binding-protein-specific, in that IGFBP-1 had detectable stimulatory effects, and IGFBP-3,

126 C cultures, the same concentration of native IGFBP-1 had no inhibitory effect.

127 ays a role in placentation and suggests that IGFBP-1 has a pathological role in preeclampsia, a disor

128 IGFBP-1 has been proposed as the acute regulator of IGF

129 nsulin-like growth factor binding protein 1 (IGFBP-1) have a high level of sequence identity with the

130 factor 1 (IGF-I) and IGF binding protein 1 (IGFBP-1) have recently been discovered by phage display

131 tionship was found for highly phosphorylated IGFBP-1 (hpIGFBP-1) concentration (known macrovascular d

132 uggesting that this HRE is functional in the IGFBP-1 hypoxia response.

133 ium] and serum IGF-I, IGF binding protein 1 (IGFBP-1), IGF binding protein 3 (IGFBP-3), and the IGF-I

134 Exercise also significantly increased IGFBP-1 in both control subjects and subjects with CF.

135 onstrated by increased expression of hepatic IGFBP-1 in IL-6 transgenic and following injection of IL

136 To assess the functional role of IGFBP-1 in liver regeneration, mice with a targeted disr

137 We assessed IGFBP-1 in relation to birth weight, maternal weight gai

138 nes of mice expressed high concentrations of IGFBP-1 in serum and tissues; however, human IGFBP-1 tra

139 Almost all of the IGFBP-1 in serum from the human IGFBP-1 transgenic mice

140 igated the hypothesis that hypoxia regulates IGFBP-1 in the human fetus in vivo and IGFBP-1 gene expr

141 glycemic control, suggesting a dual role for IGFBP-1 in the regulation of IGF actions in type 2 diabe

142 he first demonstration of the involvement of IGFBP-1 in the regulation of in vivo mitogenic signaling

143 Most of the rat IGFBP-1 in the serum of the mice expressing the rat IGFB

144 osphorylation state of human IGFBP-1 and rat IGFBP-1 in these transgenic mice.

145 The phosphorylation status of IGFBP-1 in transgenic mouse serum was analyzed by nonden

146 kinase activity phosphorylated mouse and rat IGFBP-1 in vitro, but it did not phosphorylate human IGF

147 re to IGF-I stimulated transglutamination of IGFBP-1 in vitro.

148 To investigate the physiological role of IGFBP-1 in vivo, transgenic mice have been generated usi

149 factor-I (IGF-I), and IGF binding protein-1 (IGFBP-1) in 14 subjects with CF (10.5 +/- 0.8 yr of age)

150 an-specific expression of albumin, Hnf-4 and Igfbp-1, in a set of mouse organ cDNA populations and c-

151 GFBP-1(-/-) mice with a preoperative dose of IGFBP-1 induced MAPK/ERK activation and C/EBP beta expre

152 2 was added in molar excess, suggesting that IGFBP-1 inhibits embryonic growth and development by bin

153 n its phosphorylation status; phosphorylated IGFBP-1 inhibits IGF actions whereas the nonphosphorylat

154 some proliferator-activated receptor alpha), IGFBP-1 (insulin-like growth factor binding protein 1),

155 Thus, IGFBP-1/integrin beta1/Src/FAK pathway has a crucial rol

156 estigate functionality, a 372-bp fragment of IGFBP-1 intron 1, containing putative HREs, was placed 5

157 that contain a multimerized PEPCK IRE or an IGFBP-1 IRE and this stimulation is repressed by insulin

158 fails to activate transcription through the IGFBP-1.IRE, and inhibits activation of the IGFBP-1 prom

159 and AFX, activate transcription through the IGFBP-1.IRE; this effect is inhibited by the viral oncop

160 binding to mutant versions of the PEPCK and IGFBP-1 IREs and the ability of these elements to mediat

161 lass of Fox proteins, binds to the PEPCK and IGFBP-1 IREs in a manner that correlates with the abilit

162 Therefore, the PEPCK and IGFBP-1 IREs mediate FKHRL1-induced transcription and it

163 revious mutational analyses of the PEPCK and IGFBP-1 IREs revealed mutations which do not affect the

164 ability of mutant versions of the PEPCK and IGFBP-1 IREs to bind FKHRL1 and their ability to mediate

165 Mutation of the IGFBP-1 IRSs abolished insulin inhibition in the presenc

166 In conclusion, IGFBP-1 is a substrate for tissue transglutaminase and T

167 Because regulation of IGFBP-1 is abnormal in type 1 diabetes, we examined the

168 ur data also demonstrate that amniotic fluid IGFBP-1 is derived almost exclusively from maternal sour

169 IGFBP-1 is elevated in fetuses with long-term, chronic h

170 The synthesis of IGFBP-1 is suppressed by insulin, and administration of

171 IGF binding protein-1 (IGFBP-1) is a downstream target of insulin and inhibits

172 nsulin-like growth factor binding protein 1 (IGFBP-1) is a hypoxia-inducible gene that plays an impor

173 nsulin-like growth factor binding protein 1 (IGFBP-1) is a potentially interesting marker for liver f

174 IGF binding protein-1 (IGFBP-1) is a secretory product of decidualized endometr

175 tro with cultured zebrafish embryonic cells, IGFBP-1 itself had no mitogenic activity, but it inhibit

176 We conclude that the mouse IGFBP-1 kinase activity cannot phosphorylate human IGFBP

177 urthermore, reintroduction of IGFBP-1 to the IGFBP-1 knocked-down embryos restored the hypoxic effect

178 Umbilical artery IGFBP-1 levels (mean +/- SEM) from term babies with resp

179 001) and was also negatively associated with IGFBP-1 levels (OR(q5-q1) = 0.37 [0.18-0.73]; P trend =

180 e an inverse association between circulating IGFBP-1 levels and cardiovascular risk factors.

181 Furthermore, IGFBP-1 levels are lower in subjects with overt macrovas

182 verse relationship between serum insulin and IGFBP-1 levels in glucoregulation and that sustained dys

183 U.S. prospective cohort studies, low plasma IGFBP-1 levels significantly predicted an increased risk

184 of diabetes and retinopathy had higher total IGFBP-1 levels than those with shorter disease duration.

185 In summary, maternal IGFBP-1 levels were higher in diabetic than in normal pr

186 IGFBP-1 levels were similar in normal (n = 12) and acute

187 s underlie the favorable association of high IGFBP-1 levels with insulin sensitivity and whether thes

188 mRNA in the endothelium and decreased serum IGFBP-1 levels.

189 gh-fat diet, which correlated with decreased IGFBP-1 levels.

190 lin B1 expression was delayed and reduced in IGFBP-1(-/-) livers, whereas cyclin D1 expression was no

191 nonphosphorylated and lesser-phosphorylated IGFBP-1 (lpIGFBP-1) were unrelated to macrovascular dise

192 The phosphorylation state of human IGFBP-1 may account for part of the phenotypic differenc

193 gest that the RGD integrin-binding domain of IGFBP-1 may be a promising candidate for therapeutic dev

194 of the different phosphorylated isoforms of IGFBP-1 may increase the usefulness of IGFBP-1 as a pred

195 ting concentrations of highly phosphorylated IGFBP-1 may protect against the development of hypertens

196 n and C/EBP beta expression, suggesting that IGFBP-1 may support liver regeneration at least in part

197 The hypothesis that elevated IGFBP-1 mediates hypoxia-induced embryonic growth retard

198 of hepatocyte apoptosis, IGFBP-1(-/-) mice, IGFBP-1(+/+) mice, and mice pretreated with Ab's against

199 IGFBP-1(-/-) mice also displayed increased injury in a t

200 Although IGFBP-1(-/-) mice demonstrated normal development, they

201 Treatment of IGFBP-1(-/-) mice with a preoperative dose of IGFBP-1 in

202 direct stimulation of hepatocyte apoptosis, IGFBP-1(-/-) mice, IGFBP-1(+/+) mice, and mice pretreate

203 effect on weight gain and hepatic IGF-1 and IGFBP-1 mRNA levels, compared with sham-operated pair-fe

204 Insulin lowers IGFBP-1 mRNA levels, inhibits IGFBP-1 promoter activity,

205 nsulin-like growth factor binding protein-1 (IGFBP-1) mRNA in the endothelium and decreased serum IGF

206 so shown to catalyze the formation of native IGFBP-1 multimers, however, Q66A/Q67A IGFBP-1 failed to

207 An IGFBP-1 mutant in which Gln(66)-Gln(67) had been altered

208 IGFBP-1 normally circulates as a single, highly phosphor

209 ates the inhibitory effect of phosphorylated IGFBP-1 on IGF-I stimulated 3T3-L1 cell proliferation.

210 nucleotide probes containing an IRS from the IGFBP-1 or PEPCK gene form a similar complex with hepati

211 Unlabeled competitors containing the IGFBP-1 or PEPCK IRS or a binding site for C/EBP protein

212 e have been generated using either the human IGFBP-1 or rat IGFBP-1 transgene.

213 IGFBP-1-overexpressing mice exhibited postprandial hyper

214 Aortic rings from IGFBP-1-overexpressing mice were hypocontractile in resp

215 Decidual IGFBP-1 overexpression has a marked effect on placental

216 Endogenous fetal IGFBP-1 overexpression is associated with a transient im

217 ld higher IGF-2 (P < 0.006), 5.9-fold higher IGFBP-1 (P < 0.02), and 2.5-fold higher IGFBP-3 (P < 0.0

218 se association was independently modified by IGFBP-1 (p for interaction=0.011).

219 itivity to remifentanil (SaO(2), P = 0.0440; IGFBP-1, P = 0.0013).

220 ino acid substitutions between the EPO-R and IGFBP-1 peptides have been analyzed to assess the degree

221 at hypoxia and rapamycin treatment increased IGFBP-1 phosphorylation at Ser98/Ser101/Ser119/Ser174 bu

222 e have therefore examined the IGF system and IGFBP-1 phosphorylation status, using specifically devel

223 IGFBP-1 phosphorylation, which markedly increases its af

224 s the first compelling in vivo evidence that IGFBP-1 plays a role in placentation and suggests that I

225 Our data suggest that IGFBP-1 plays an important and potentially beneficial ro

226 Dephosphorylated IGFBP-1 polymerized more rapidly and to a greater extent

227 xpressing neurons versus a reduced number of IGFBP-1 positive neurons.

228 Although the mutant IGFBP-1 potently inhibited IGF-I stimulated protein synt

229 AK localizes to the nucleus and Src triggers IGFBP-1 production.

230 hepatic and nonhepatic cells, IL-6 -mediated IGFBP-1 promoter activation was via an intact hepatocyte

231 Cotransfection of mouse FKHR increased IGFBP-1 promoter activity 2-3-fold in H4IIE rat hepatoma

232 Insulin lowers IGFBP-1 mRNA levels, inhibits IGFBP-1 promoter activity, and activates PKB/Akt in HepG

233 on and, consequently, insulin suppression of IGFBP-1 promoter activity.

234 promoter and mediates insulin inhibition of IGFBP-1 promoter activity.

235 IGFBP-1.IRE, and inhibits activation of the IGFBP-1 promoter by glucocorticoids.

236 Although the zebra fish IGFBP-1 promoter contains 13 consensus hypoxia response

237 The IGFBP-1 promoter contains two IRSs each of which is suff

238 ficient to mediate effects of insulin on the IGFBP-1 promoter in a nonadditive fashion.

239 AS greatly reduced the responsiveness of the IGFBP-1 promoter to hypoxia and HIF-1.

240 ely blocked IL-6-mediated stimulation of the IGFBP-1 promoter via the HNF-1 site.

241 ice a 970-bp region from -776 to +151 of the IGFBP-1 promoter was sufficient for tissue-specific and

242 tivator complex to an FKH factor site in the IGFBP-1 promoter, which allows the cell to integrate the

243 nsulin-like growth factor-binding protein-1 (IGFBP-1) promoter and mediates insulin inhibition of IGF

244 nsulin-like growth factor binding protein-1 (IGFBP-1) promoter.

245 nsulin-like growth factor binding protein-1 (IGFBP-1) promoters have been proposed to contribute to r

246 IGFBP-1 protein and mRNA increased 8- and 12-fold, respe

247 cking antibody or neutralization of IGF-I by IGFBP-1 reduced cell motility.

248 To investigate IGFBP-1 regulation by hypoxia in vitro, HepG2 cells were

249 e residues were changed to the corresponding IGFBP-1 sequence were determined.

250 articipants in the lowest quartile of plasma IGFBP-1 showed an elevated risk of pancreatic cancer.

251 Knockdown of IGFBP-1 significantly alleviated the hypoxia-induced gro

252 Posttranslational phosphorylation of IGFBP-1 significantly increases its affinity for IGF-I a

253 norhabditis elegans protein DAF-16 binds the IGFBP-1 small middle dotIRE with specificity similar to

254 cells, in contrast to Schwann cells, release IGFBP-1 that activates the Src/FAK pathway, via integrin

255 important post-translational modification of IGFBP-1 that regulates cellular responses to IGF-I.

256 tion correlated with the amount of monomeric IGFBP-1 that was present.

257 tified as major specificity determinants for IGFBP-1: the corresponding alanine mutations, E3A and F4

258 nts in the three highest quartiles of plasma IGFBP-1, those in the lowest quartile experienced a rela

259 cleaved IGFBP-5 but had no activity against IGFBP-1 through -4.

260 ore, we demonstrated that RTEF-1 upregulates IGFBP-1 through selective binding and promotion of trans

261 The RGD integrin-binding domain of IGFBP-1, through integrin engagement, focal adhesion kin

262 Total IGFBP-1 (tIGFBP-1), which is predominantly highly phosph

263 insulin-like growth factor-binding proteins (IGFBP-1 to -6) are a family of structurally homologous p

264 125I-labeled recombinant human IGFBPs (125I-IGFBP-1 to -6) in the presence of the cross-linking agen

265 portant determinant of the capacity of human IGFBP-1 to inhibit IGF-1 actions in vivo.

266 This capacity of IGFBP-1 to inhibit or stimulate IGF-I actions correlates

267 suppressed by insulin, and administration of IGFBP-1 to rats results in impaired glucose metabolism.

268 Furthermore, reintroduction of IGFBP-1 to the IGFBP-1 knocked-down embryos restored the

269 in, and mediates insulin inhibition of basal IGFBP-1 transcription in an IRS-dependent manner.

270 TEF-1 expression and significantly inhibited IGFBP-1 transcription in endothelial cells in a dose-dep

271 When the human IGFBP-1 transgene was transfected into Hepa 1-6 cells, a

272 However, when the rat IGFBP-1 transgene was transfected into these cells, phos

273 erated using either the human IGFBP-1 or rat IGFBP-1 transgene.

274 IGFBP-1 in serum and tissues; however, human IGFBP-1 transgenic mice did not show glucose intolerance

275 intrauterine growth retardation, whereas rat IGFBP-1 transgenic mice showed fasting hyperglycemia and

276 t all of the IGFBP-1 in serum from the human IGFBP-1 transgenic mice was present as a nonphosphorylat

277 and TGF-beta1 expression were suppressed by IGFBP-1 treatment, supporting their role in the apoptoti

278 Human IGFBP-1 undergoes serine phosphorylation, and this enhan

279 reaction and the effect of polymerization of IGFBP-1 upon IGF-I action.

280 Evidence for a biologic role of IL-6 in IGFBP-1 upregulation was demonstrated by increased expre

281 In multiple regression analysis, IGFBP-1 was independently and negatively related to fast

282 Similarly, IGFBP-1 was inversely associated with prostate cancer ri

283 Age- and sex-adjusted IGFBP-1 was inversely related to fasting insulin and pro

284 In contrast, binding of IGFBP-1 was more sensitive to alanine substitutions in I

285 The influence of plasma IGFBP-1 was most marked among participants who never smo

286 in the serum of the mice expressing the rat IGFBP-1 was phosphorylated.

287 transfected into Hepa 1-6 cells, all of the IGFBP-1 was secreted in the nonphosphorylated form.

288 oxic conditions, litter size was reduced and IGFBP-1 was up-regulated in maternal serum and in fetal

289 A serum hypoxia marker (IGFBP-1) was associated with hypoalgesia and increased p

290 knockdown, small inhibitors and recombinant IGFBP-1, we demonstrate that schwannoma cells, in contra

291 tide and lower levels of prediagnosis plasma IGFBP-1 were associated with increased mortality.

292 ed into these cells, phosphorylated forms of IGFBP-1 were secreted.

293 mice, and mice pretreated with Ab's against IGFBP-1 were treated with a normally sublethal dose of F

294 07, P < 0.05), and significant predictors of IGFBP-1 were vegetable protein (beta = 0.49, P < 0.05) a

295 her insulin growth factor binding protein-1 (IGFBP-1) were associated with higher analgesic sensitivi

296 1 kinase activity cannot phosphorylate human IGFBP-1, whereas it can phosphorylate rat IGFBP-1.

297 clude that alpha(2)M is a binding protein of IGFBP-1 which modifies IGF-I/IGFBP-1 actions resulting i

298 nsulin-like growth factor-binding protein-1 (IGFBP-1), which is expressed and released from central n

299 nsulin-like growth factor binding protein 1 (IGFBP-1), which results in elevated levels in serum of I

300 n, bp1-01 competes with IGF-I for binding to IGFBP-1, which leads to release of free IGF-I from IGF-I

301 IGF-I/IGFBP-3 with lactose and calcium; and IGFBP-1 with vegetable protein.