ライフサイエンスコーパス: IGFBP-3

1 nsulin-like growth factor binding protein-3 (IGFBP-3).

2 nsulin-like growth factor-binding protein-3 (IGFBP-3).

3 nsulin-like growth factor binding protein 3 (IGFBP-3).

4 influence insulin sensitivity, probably via IGFBP-3.

5 BP-2 and an approximately 29-kDa fragment of IGFBP-3.

6 0) for IGF-I and 3.31 (1.10, 9.98) for IGF-I/IGFBP-3.

7 e approximately 29-kDa band as a fragment of IGFBP-3.

8 IGF-I variant peptide that does not bind to IGFBP-3.

9 jection on day 1 and a daily IT injection of IGFBP-3.

10 ship in vitro and in vivo between NKX3.1 and IGFBP-3.

11 s the relationship between reduced IGF-I and IGFBP-3.

12 t growth is by transcriptional repression of IGFBP-3.

13 arrest and apoptosis including p21(CIP1) and IGFBP-3.

14 nd an injection of either placebo or rhIGF-I/IGFBP-3 (0.1-0.8 mg x kg(-1) x day (-1)) was given subcu

15 FBP-2 (1.18; 1.06-1.31; P(trend) < 0.01) and IGFBP-3 (1.27; 1.19-1.36; P(trend) < 0.001), but not IGF

16 racellular and mutated the C-terminal NLS of IGFBP-3, (228)KGRKR(232), to MDGEA.

17 BP-1 had detectable stimulatory effects, and IGFBP-3, -4, -5, and -6 inhibited RPE responses.

18 ic RPE have detectable levels of message for IGFBP-3, -5, and -6.

19 nsulin-like growth factor-binding protein-3 (IGFBP-3), a major regulator of endocrine actions of IGFs

20 nsulin-like growth factor binding protein-3 (IGFBP-3), a secreted protein, has the intrinsic ability

21 pendent phosphorylation in the regulation of IGFBP-3 action.

22 ear localization may play important roles in IGFBP-3 action.

23 IGFBP-3 activation was significantly reduced following t

24 nsulin-like growth factor binding protein-3 (IGFBP-3) activation in retinal endothelial cells (REC) t

25 cient serotype 5 adenovirus expressing human IGFBP-3 (Ad3), IGFBP-5 (Ad5), or no complementary DNA (c

26 t adenovirus expressing human IGFBP-5 (Ad5), IGFBP-3 (Ad3), or no cDNA (cAd) to wild-type mice.

27 nsulin-like growth factor binding protein 3 (IGFBP-3), adiponectin, C-reactive protein (CRP), and int

28 ted mitochondria at a 4-fold lower dose than IGFBP-3 alone.

29 ced by the nonsecreted NLS mutant (YFP-MDGEA-IGFBP-3) alone and when the IGF-binding site also had be

30 IGFBP-3 also reduced the retinal ceramide/sphingomyelin

31 nsulin-like growth factor-binding protein 3 (IGFBP-3) among 517 cases and 790 controls from the US Se

32 Our data demonstrate that the IGFBP-3 and BAX interaction activates germ cell apoptosi

33 particularly elevated calcium with IGF-I and IGFBP-3 and elevated vegetable protein with IGFBP-1-and,

34 er, the IGFBP3 signal (associated with total IGFBP-3 and IGF-II levels) colocalizes with an associati

35 Expression analysis of IGFBP-3 and IGFBP-3R indicates that the IGFBP-3/IGFBP-3R

36 y expressed in sensitive cell lines, whereas IGFBP-3 and IGFBP-6 were highly expressed in resistant l

37 ociations between plasma levels of IGF-1 and IGFBP-3 and laparoscopically confirmed endometriosis in

38 (a), a measure of lipolysis, between rhIGF-I/IGFBP-3 and placebo.

39 vestigated serum concentrations of IGF-1 and IGFBP-3 and their molar ratio in relation to T2DM incide

40 lycemia to determine the interaction between IGFBP-3 and TNF-alpha, as data indicate that both protei

41 nist we have reported previously to regulate IGFBP-3 and TNF-alpha.

42 These findings suggest that serum levels of IGFBP-3 (and possibly IGF-I) are associated with the rat

43 hat downregulation of IGF-binding protein 3 (IGFBP-3) and -4, the negative regulators of IGF-I recept

44 nship of measured serum levels with SHR (for IGFBP-3) and birth weight (for IGFBP-5) than with height

45 ited markedly reduced IGF-binding protein 3 (IGFBP-3) and IGFBP-4 RNA.

46 protein 1 (IGFBP-1), IGF binding protein 3 (IGFBP-3), and the IGF-I:IGFBP-3 molar ratio in adolescen

47 (95% CI: 1.00, 1.76; P for trend = 0.04) for IGFBP-3, and 0.77 (95% CI: 0.57, 1.03; P for trend = 0.0

48 with several IGF-binding proteins (IGFBP-2, IGFBP-3, and IGFBP-5).

49 IGF-1, IGFBP-3, and the molar ratio appeared to be positively a

50 Especially VDR target genes CYP24A1, IGFBP-3, and TRPV6 were negatively regulated by GW0742.

51 ction of saline; (iii) daily IT injection of IGFBP-3; and (iv) a GnRH-A injection on day 1 and a dail

52 Both forms of IGFBP-3 are also without mitogenic effects alone or in c

53 s-promoting and growth-inhibitory actions of IGFBP-3 are completely abrogated in the absence of catal

54 The initial screening showed that IGF-1 and IGFBP-3 are differentially expressed in CAV compared wit

55 GF-independent, antiproliferative actions of IGFBP-3 are largely unknown.

56 nsulin-like growth factor-binding protein-3 (IGFBP-3) are involved in cell replication, proliferation

57 Future studies are needed for development of IGFBP-3 as a new line of antiangiogengic cancer drug.

58 These studies support consideration of IGFBP-3 as a novel agent to restore the function of inju

59 IGFBP-3 as well as BAX induced release of cytochrome c a

60 sma 25-hydroxyvitamin D (25(OH)D) and IGF-1, IGFBP-3 as well as C-peptide levels in 499 cases and 992

61 This article presents IGF-binding protein-3 (IGFBP-3) as a new modulator of apoptosis and survival si

62 the IGF-I association was attenuated but the IGFBP-3 association was not.

63 er co-immunoprecipitation with BAX antibody, IGFBP-3 association with BAX was demonstrated in total a

64 Intact IGFBP-3 attenuated extracellular matrix contraction in r

65 ge in TRAMP mice via modulation of tumor IGF-IGFBP-3 axis and cell cycle regulation, and therefore it

66 nsulin-like growth factor binding protein-3 (IGFBP-3) belongs to a family of six IGF binding proteins

67 Dot blot studies further validated the BAX-IGFBP-3 binding in vitro.

68 iscovered that in addition to IGF1 and IGF2, IGFBP-3 binds bFGF, HGF, neuregulin, and PDGF AB with na

69 whereas overexpression of IGFBP-3R enhanced IGFBP-3 biological effects.

70 We observed that IGFBP-3 blocked tumor angiogenesis and growth in non-sma

71 1, rs2854746 (Gly32Ala), was associated with IGFBP-3 blood levels (P(adj) = 8.8 x 10(-43)) after adju

72 P3 promoter polymorphism A-202C (rs2854744); IGFBP-3 blood levels were 6.3% higher for each minor all

73 tein (BP) 1, and IGFBP3 genes with IGF-I and IGFBP-3 blood levels, and prostate cancer (PCa) risk, am

74 dentified SNPs significantly associated with IGFBP-3 blood levels, but none of these alter PCa risk;

75 GF-1 deficiency (LID), ALS knockout (ALSKO), IGFBP-3 (BP3) knockout, and a triply deficient LID/ALSKO

76 n membrane protein and binds specifically to IGFBP-3 but not other IGFBP species.

77 compared with 1.7 (1.6, 2.0); P = 0.02], and IGFBP-3 by 6% (mean +/- SEM: 2420 +/- 29 compared with 2

78 In vitro phosphorylation of IGFBP-3 by DNA-dependent protein kinase (DNA-PK) has bee

79 IGFBP-3 can induce changes in podocyte actin cytoskeleto

80 Immunoprecipitation for total and phospho-IGFBP-3, cell proliferation and cell death measurements

81 ith IGF-I concentration after adjustment for IGFBP-3 concentration (P = 1.9 x 10(-26)).

82 ed genome-wide significant associations with IGFBP-3 concentration (rs1065656, chromosome 16p13.3, P

83 xplained 6.5% of the population variation in IGFBP-3 concentration.

84 d significantly higher circulating IGF-I and IGFBP-3 concentrations and faster growth rates than cont

85 there were no associations between IGF-1 or IGFBP-3 concentrations and risk of testicular germ-cell

86 was a transient increase in plasma IGF-I and IGFBP-3 concentrations at fetal 90 d in prenatal T-treat

87 Circulating IGF-I and IGFBP-3 concentrations predict anthropometric traits and

88 IGFBP3 gene region on chromosome 7p12.3 with IGFBP-3 concentrations using a significance threshold of

89 s (e.g. rs11977526) that was associated with IGFBP-3 concentrations was also associated with the oppo

90 Plasma IGF-I and IGF binding protein 3 (IGFBP-3) concentrations and molar ratio of IGF-I to IGFB

91 IGFBP-3 contains a nuclear localization signal (NLS), an

92 Recent epidemiologic studies suggest that IGFBP-3 contributes to cancer risk protection in a varie

93 result of lipotoxicity, and whether altered IGFBP-3 could affect pathways that are involved in hepat

94 To assess the effects of IGFBP-3 deficiency on prostate cancer development, we cr

95 3) IGFBP-3 deficiency resulted in increased linear growth.

96 re of palmitate-treated THP-1 macrophages to IGFBP-3-deficient conditioned medium led to a 20-fold in

97 In cancer cells, IGFBP-3 directly interacted with Erk1/2, leading to inac

98 s undertaken to investigate the mechanism of IGFBP-3 effects on EPC function and how IGFBP-3 mediates

99 Cell lysates were processed for IGFBP-3 ELISA analyses and Western blotting to measure c

100 ared with control, which was confirmed by an IGFBP-3 enzyme-linked immunosorbent assay.

101 We previously found that IGFBP-3 exerts its cytotoxic effects on A549 (p53 wild-t

102 that mice that are genetically deficient in IGFBP-3 exhibit weaker growth of primary prostate tumors

103 IGFBP-3 exposure also led to the redistribution of vasod

104 Intravitreal injection of IGFBP-3-expressing plasmid into lasered GFP chimeric mic

105 vitreal injection of an endothelial-specific IGFBP-3-expressing plasmid resulted in increased differe

106 , small interfering RNA-induced knockdown of IGFBP-3 expression partially reversed the attenuation of

107 Increased IGFBP-3 expression reduced the number of activated micro

108 BAX-associated IGFBP-3 expression was increased in mitochondria after t

109 DNA-PK is required for Compound 49b-induced IGFBP-3 expression, leading to inhibition of REC cell de

110 ells are mediated, in part, by activation of IGFBP-3 expression.

111 circulation through enhancing VDR-regulated IGFBP-3 expression.

112 y, tumor grade, disease stage, and IGF-II or IGFBP-3 expression.

113 nsulin-like growth factor binding protein-3 (IGFBP-3) expression.

114 egulated expression in both assays (Igfbp-6, Igfbp-3, Fbn2, Ntrk3, Agpt4, Dmp1, and Mmp13).

115 Growth factor sequestration by IGFBP-3-Fc enhances the activity of EGFR inhibitors by d

116 bition of tumor growth in vivo with adjuvant IGFBP-3-Fc with erlotinib versus erlotinib after treatme

117 ere similarly unresponsive to IGFBP-3 or the IGFBP-3 fragment alone or in combination with IGF-I or I

118 erhaps identical with a previously described IGFBP-3 fragment in plasma with reduced growth factor af

119 stion revealed that the approximately 29-kDa IGFBP-3 fragment is a glycoprotein with a peptide core o

120 on in response to IGF-I and IGF-II while the IGFBP-3 fragment modulated cell responses to IGF-II only

121 The vitreous-type IGFBP-3 fragment was isolated from normal human plasma a

122 sional gel electrophoresis revealed that the IGFBP-3 fragments in vitreous and plasma have virtually

123 IGFBP-3 further inhibits TNF-alpha, CRP and high glucose

124 Specifically, CDX2 binds to the IGFBP-3 gene promoter and can repress IGFBP-3 transcript

125 SRC-3 in VDR-mediated transactivation of the IGFBP-3 gene.

126 Both IGFBPs retain biological activity, and IGFBP-3 has one or more glycosylation sites with a prote

127 In the absence of DNA-PK activity, IGFBP-3 has reduced nuclear accumulation and is unable t

128 nsulin-like growth factor binding protein-3 (IGFBP-3) has been reported to suppress tumor growth and

129 Some antiproliferative actions of IGFBP-3 have been reported to be independent of IGFs, bu

130 Only IGFBP-3, however, was significantly associated with AIDS

131 After controlling for IGFBP-3, IGF-II was no longer associated (0.99; 0.91-1.0

132 Our data suggest that the IGFBP-3/IGF pathway is involved in the pathogenesis of l

133 elopment and regeneration, including PDGF-A, IGFBP-3, IGFBP-2, and IGF-1.

134 s of IGFBP-3 and IGFBP-3R indicates that the IGFBP-3/IGFBP-3R axis is impaired in breast and prostate

135 Thus, the IGFBP-3/IGFBP-3R axis may provide therapeutic and progno

136 f caspase-8 expression or activity inhibited IGFBP-3/IGFBP-3R-induced apoptosis.

137 hese findings suggest that reduced levels of IGFBP-3 in circulation and reduced expression of IGFBP-3

138 l IGFBP-3 levels and increase in proteolyzed IGFBP-3 in circulation when compared to their normal cou

139 Silencing IGFBP-3 in Huh7 cells enhanced JNK and NF-kappaB activit

140 ibodies demonstrate the presence of IRBP and IGFBP-3 in isolated retinas.

141 P-3 in circulation and reduced expression of IGFBP-3 in macrophages in obesity may result in suppress

142 ovel regulatory mechanism for the actions of IGFBP-3 in prostate cancer and show phosphorylation of S

143 t roles for circulating IGF-II, IGFBP-2, and IGFBP-3 in PSA-detected prostate cancer, in support of r

144 Compound 49b required DNA-PK to activate IGFBP-3 in REC.

145 Our findings established a function for IGFBP-3 in suppressing metastasis in prostate cancer, an

146 ectional insulin, IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in the Boyd Orr cohort (n = 182 men, 223 women).

147 fibroblasts were stimulated with TGFbeta or IGFBP-3 in the presence or absence of specific small int

148 To understand better the role of IGFBP-3 in the retina, IGFBP-3 knockout (KO) mice were e

149 nsulin-like growth factor binding protein-3 (IGFBP-3) in male germ cell apoptosis.

150 nsulin-like growth factor binding protein-3 (IGFBP-3) in mouse retina.

151 In summary, IGFBP-3 increased differentiation of GFP(+) HSCs into pe

152 IGFBP-3 increased endothelial NO synthase expression in

153 ) concentrations and molar ratio of IGF-I to IGFBP-3 increased, whereas IGFBP-2 decreased throughout

154 It was found that IGFBP-3 increments the level of TGF-beta1-induced phosph

155 cell death receptor and is essential for the IGFBP-3-induced apoptosis and tumor suppression.

156 Knockdown of IGFBP-3R attenuated IGFBP-3-induced caspase activities and apoptosis, wherea

157 o studies demonstrate that IGFBP-3R mediates IGFBP-3-induced caspase-8-dependent apoptosis in various

158 ndependent Erk1/2 inactivation and decreased IGFBP-3-induced Egr-1 expression block the autocrine and

159 y of cancers, and a polymorphic variation of IGFBP-3 influences cancer risk, although other studies v

160 In vitro, IGFBP-3 inhibited both vascular endothelial growth facto

161 d to REC, they worked antagonistically, with IGFBP-3 inhibiting apoptosis and TNF-alpha promoting apo

162 In human adipocytes, we show that IGFBP-3 inhibits TNF-alpha-induced NF-kappaB activity in

163 e interval (CI): 0.61, 1.27; Ptrend = 0.48), IGFBP-3 (IRR = 1.12, 95% CI: 0.80, 1.57; Ptrend = 0.51),

164 FBP-3: IRR = 1.85, 95% CI: 1.08, 3.16; IGF-1:IGFBP-3: IRR = 1.57, 95% CI: 0.85, 2.88) but not among w

165 draw (IGF-1: IRR = 1.60, 95% CI: 0.86, 2.98; IGFBP-3: IRR = 1.85, 95% CI: 1.08, 3.16; IGF-1:IGFBP-3:

166 e insulin-like growth factor binding protein IGFBP-3 is a proapoptotic and antiangiogenic protein in

167 Epidemiologic studies suggest that low IGFBP-3 is associated with greater risk of aggressive, m

168 One of the IGF-independent functions of IGFBP-3 is its role as an anti-inflammatory molecule.

169 matic comparisons indicate that the vitreous IGFBP-3 is similar to and perhaps identical with a previ

170 ear localization signal (NLS), and exogenous IGFBP-3 is translocated into the nucleus, suggesting tha

171 nsulin-like growth factor binding protein-3 (IGFBP-3) is a biologically active fragment of the intact

172 IGF-binding protein-3 (IGFBP-3) is a liver-derived, anti-inflammatory molecule

173 otein IGF-binding protein (IGFBP)-3 (rhIGF-I/IGFBP-3) is a novel formulation that has been shown to i

174 16-week-old, liver-specific IGF-1-deficient, IGFBP-3 knock-out (BP3KO) and acid-labile subunit knock-

175 d ELISA analyses were done to verify PKA and IGFBP-3 knockdown, as well as to measure apoptotic marke

176 nd better the role of IGFBP-3 in the retina, IGFBP-3 knockout (KO) mice were evaluated for neuronal,

177 Prostates in IGFBP-3 knockout mice (IGFBP-3KO mice) failed to undergo

178 and oscillatory potential amplitudes in the IGFBP-3 KO mice, corresponding to increased apoptosis.

179 the ganglion cell layer were reduced in the IGFBP-3 KO mice.

180 constructs, Western blots indicated that YFP-IGFBP-3 lacking a signal peptide was cell-associated and

181 d yellow fluorescent protein (YFP) to mature IGFBP-3 lacking its signal peptide so that it would rema

182 reased over that in SRC-3(-/-) mice, but the IGFBP-3 level failed to increase proportionally, indicat

183 ease proportionally, indicating that the low IGFBP-3 level is a responsible factor that limits the IG

184 IGFBP-3 level remained positively associated with T2DM i

185 Low IGF-I levels (Ptrend= .02) and high IGFBP-3 levels (Ptrend= .02) were associated with rapid

186 n obese adolescents show a decrease in total IGFBP-3 levels and increase in proteolyzed IGFBP-3 in ci

187 Serum IGF-I and IGFBP-3 levels in LID and LID-TRAMP mice were measured u

188 least in part by an increase in circulating IGFBP-3 levels in the transgenic animals.

189 he general study population, although higher IGFBP-3 levels might raise T2DM risk independent of IGF-

190 It was not known whether IGFBP-3 levels were altered in NAFLD, whether such alter

191 to prevent REC apoptosis through increasing IGFBP-3 levels, which are reduced in response to hypergl

192 tion was associated with drastically reduced IGFBP-3 levels.

193 beneficial effects on diabetes risk, whereas IGFBP-3 may have adverse effects.

194 ts anti-inflammatory functions and therefore IGFBP-3 may present itself as a therapeutic for obesity-

195 Thus, endothelial expression of IGFBP-3 may represent a physiologic response to injury a

196 IGFBP-3 mediated the induction of TN-C by TGFbeta.

197 IGFBP-3-mediated NO generation required high-density lip

198 The contribution of bone marrow cells in the IGFBP-3-mediated response was examined using green fluor

199 m of IGFBP-3 effects on EPC function and how IGFBP-3 mediates cytoprotection following vascular injur

200 nsulin-like growth factor-binding protein 3 (IGFBP-3) might raise the risk of type 2 diabetes mellitu

201 Intact IGFBP-3 modulates Muller cell tractional force generatio

202 I: 0.80, 1.57; Ptrend = 0.51), and the IGF-1:IGFBP-3 molar ratio (IRR = 0.94, 95% CI: 0.66, 1.34; Ptr

203 F binding protein 3 (IGFBP-3), and the IGF-I:IGFBP-3 molar ratio in adolescent females.

204 in LNCaP cells, NKX3.1 expression increased IGFBP-3 mRNA and protein expression.

205 phosphorylation and GH-stimulated IGF-1 and IGFBP-3 mRNA expression.

206 In prostates of Nkx3.1 gene-targeted mice Igfbp-3 mRNA levels correlated with Nkx3.1 copy number.

207 Furthermore, IGFBP-3 mRNA was reduced in SRC-3(-/-) mice.

208 nsulin-like growth factor binding protein-3 (IGFBP-3) mRNA expression 10-fold as determined by expres

209 ere done after transfection with the S(156)A IGFBP-3 mutation (key phosphorylation site involved in D

210 s of blood serum IGF-I, IGF-II, IGFBP-2, and IGFBP-3 obtained at recruitment.

211 Direct induction of TN-C by IGFBP-3 occurred in a p38 MAP kinase-dependent manner.

212 ed that IGF-1 (odds ratio, 0.89; P=0.04) and IGFBP-3 (odds ratio, 0.09; P=0.03) are independent risk

213 we examined whether the effects of IGF-I and IGFBP-3 on insulin action are mediated through central m

214 metabolism, we conclude that the effects of IGFBP-3 on the hypothalamus involve activity mediated by

215 We investigated the effects of IGFBP-3 on tumor growth and angiogenesis utilizing a hum

216 cell apoptosis increased significantly after IGFBP-3 or GnRH-A treatment which was further enhanced b

217 s binary complexes or ternary complexes with IGFBP-3 or IGFBP-5 and an acid-labile subunit (ALS).

218 rast to this, ternary complex formation with IGFBP-3 or IGFBP-5 and the auxillary protein, acid labil

219 Taken together, our results show that IGFBP-3 or its peptide blocks hyaluronan-CD44 signaling

220 The cells were similarly unresponsive to IGFBP-3 or the IGFBP-3 fragment alone or in combination

221 of these cytoprotective effects exhibited by IGFBP-3 overexpression can result in a more stable retin

222 me-wide significant associations with higher IGFBP-3 (P = 4.4 x 10(-21)) and higher IGF-I (P = 4.9 x

223 Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays.

224 Furthermore, inhibition of IGFBP-3 partially rescues the decreased anchorage-indepe

225 as a normal affinity to IGFs but binds other IGFBP-3 partners poorly and fails to normally internaliz

226 A synthetic IGFBP-3 peptide ((215)-KKGFYKKKQCRPSKGRKR-(232)) but not

227 Administration of IGFBP-3 plasmid to mouse pups that underwent the oxygen-

228 verall, these data suggest that, if IGF-1 or IGFBP-3 plays a role in the etiology of endometriosis, i

229 tein levels of IGF-I, IGF binding protein-3 (IGFBP-3), pregnancy-associated plasma protein A (PAPP-A2

230 In the OIR model, IGFBP-3 prevented cell death of resident vascular endoth

231 The IGFBP-3 promoter activity induced by vitamin D, through

232 -like growth factor (IGF) binding protein-3 (IGFBP-3) promotes apoptosis of cancer cells by both IGF-

233 Serum IGFBP-3 protein concentrations were significantly lower

234 Treatment with the IGFBP-3 protein or its peptide resulted in increased ace

235 In a manner comparable to that of the IGFBP-3 protein, the peptide blocked hyaluronan-CD44 sig

236 < 0.001) increase in IGF-binding protein 3 (IGFBP-3) protein levels were also observed.

237 d establishes a positive correlation between IGFBP-3 proteolysis and adiposity parameters as well as

238 participants with high 25(OH)D and low IGF-1/IGFBP-3 ratio (reference group), participants with a hig

239 ipants with high 25(OH)D and low molar IGF-1/IGFBP-3 ratio and low C-peptide levels (reference group)

240 lorectal cancer associated with higher IGF-1/IGFBP-3 ratio or C-peptide levels.

241 ants with a combination of either high IGF-1/IGFBP-3 ratio or high C-peptide were at elevated risk fo

242 rence group), participants with a high IGF-1/IGFBP-3 ratio were at elevated risk of colorectal cancer

243 I: 0.57, 1.03; P for trend = 0.03) for IGF-1:IGFBP-3 ratio.

244 resses monocyte adhesion to HAEC through the IGFBP-3 receptor.

245 Addition of recombinant IGFBP-3 restored the ability of gefitinib to downregulat

246 erminal sequence data obtained from vitreous IGFBP-3 revealed that the protein is proteolytically tru

247 inhibitor or following transfection with the IGFBP-3 S(156)A mutant plasmid (P < 0.05).

248 also observed in cells transfected with the IGFBP-3 S(156)A mutant plasmid (P < 0.05).

249 se findings provide a molecular framework of IGFBP-3's IGF-independent antiangiogenic antitumor activ

250 In contrast, IGFBP-3-S156A was unable to promote apoptosis and exhibi

251 When transfected into 22RV1 cells, IGFBP-3-S165A and IGFBP-3-T170A functioned in an identic

252 Palmitate inhibited IGFBP-3 secretion by THP-1 macrophages and enhanced IL-8

253 nsulin-like growth factor binding protein-3 (IGFBP-3), semaphorin-3B, transforming growth factor (TGF

254 These data indicate that IGFBP-3 serves as an anti-inflammatory brake in hepatocy

255 Taken together, loss of IGFBP-3 signaling results in a phenotype similar to neur

256 nsulin-like growth factor binding protein 3 (IGFBP-3) signaling would produce neuronal changes in the

257 In contrast, ICV infusion of IGFBP-3 significantly impaired insulin action at the liv

258 eatment with protein kinase A (PKA) siRNA or IGFBP-3 siRNA.

259 Because IGF-I and IGFBP-3 stabilize each other, SRC-3(-/-) mice were cross

260 cers were observed in all mice regardless of IGFBP-3 status.

261 Conversely, overexpression of IGFBP-3 suppressed JNK and NF-kappaB activation and bloc

262 s they were not reflected in circulating IGF-IGFBP-3 system.

263 nsfected into 22RV1 cells, IGFBP-3-S165A and IGFBP-3-T170A functioned in an identical manner to wild-

264 nsulin-like growth factor binding protein 3 (IGFBP-3), testosterone, androstenedione, androstanediol

265 ulinemic clamp was greater following rhIGF-I/IGFBP-3 than placebo, both during the first (P = 0.008)

266 We assessed the ability of a form of IGFBP-3 that does not bind IGF-1 (IGFBP-3NB), to regulat

267 ate inhibits hepatic macrophage secretion of IGFBP-3, thereby releasing the brake and enhancing palmi

268 dependent physiological effects of IGF-I and IGFBP-3 through central mechanisms may have implications

269 line serum samples were tested for IGF-I and IGFBP-3 to determine their associations with incident cl

270 nctioned in an identical manner to wild-type IGFBP-3 to induce apoptosis.

271 Compound 49b requires active PKA and IGFBP-3 to prevent apoptosis of REC.

272 ile subunit (ALS) and IGF-binding protein 3 (IGFBP-3) to maintain its circulating concentration and e

273 to the IGFBP-3 gene promoter and can repress IGFBP-3 transcription, protein expression and secretion.

274 Conditioned media from an IGFBP-3-treated non-small cell lung cancer cell line dis

275 uncorrected P = 0.008); CTBP2-rs4962416 with IGFBP-3 (uncorrected P = 0.003); 11q13.2-rs12418451 with

276 ee potential DNA-PK phosphorylation sites in IGFBP-3 using PCR-based site-directed mutagenesis.

277 ptosis of REC may depend upon which protein (IGFBP-3 versus TNF-alpha) is active.

278 As expected, loss of IGFBP-3 was associated with increased TNF-alpha levels.

279 .14, P < 0.01), the significant predictor of IGFBP-3 was calcium (beta = 0.07, P < 0.05), and signifi

280 Serum IGFBP-3 was decreased in patients with NAFLD, whereas li

281 ith T2DM incidence-and the ratio of IGF-1 to IGFBP-3 was inversely related with T2DM incidence--in mo

282 IGFBP-3 was positively associated with diabetes (OR(q5-q

283 imaging showed that intracellular YFP-MDGEA-IGFBP-3 was predominantly cytoplasmic.

284 nsulin-like growth factor binding protein 3 (IGFBP-3) was associated with endometriosis.

285 When TNF-alpha and IGFBP-3 were applied to REC, they worked antagonisticall

286 s, we asked whether the migratory effects of IGFBP-3 were attributable to stimulation of NO generatio

287 estational weeks 10-14, both IGF-I and IGF-I/IGFBP-3 were positively associated with GDM risk; adjust

288 e vitreous, plasma, recombinant IGFBP-2, and IGFBP-3 were separated by gel electrophoresis.

289 sequently, IGF-1- and IGF-binding protein-3 (IGFBP-3) were analyzed using enzyme-linked immunosorbent

290 IGFBP-3, when combined with an ineffective dose of BAX,

291 tment significantly increased GH, IGF-I, and IGFBP-3, whereas serum cortisol decreased (P < 0.05).

292 ns were noted between mortality and IGF-I or IGFBP-3, which are two components of the IGF axis not cl

293 As the nuclear localization signal mutant IGFBP-3, which has a normal affinity to IGFs but binds o

294 IGFBP-3, which is overexpressed in fibrotic lungs, induc

295 BP-3 with TGF-beta1 because a combination of IGFBP-3 with bone morphogenic protein-7 (BMP-7), another

296 inverse), lactose, fiber, and calcium; IGF-I/IGFBP-3 with lactose and calcium; and IGFBP-1 with veget

297 e associations of insulin, IGF-I, IGF-II and IGFBP-3 with physical performance in the UK-based Caerph

298 stent evidence of associations of IGF-II, or IGFBP-3 with physical performance.

299 effect is specific for the co-stimulation of IGFBP-3 with TGF-beta1 because a combination of IGFBP-3

300 total protein, lactose, calcium, and sodium; IGFBP-3 with total fat (inverse), lactose, fiber, and ca