ライフサイエンスコーパス: IGFBP

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

2 IGFBP-1 can affect cellular functions independently of I

3 IGFBP-1 phosphorylation, which markedly increases its af

4 IGFBP-2 bound RPTPbeta, which led to its dimerization an

5 IGFBP-2 enhanced IGF-I-stimulated VSMC migration and pro

6 IGFBP-2 knockdown led to decreased PTEN tyrosine phospho

7 IGFBP-2 levels rise during rapid neonatal growth and at

8 IGFBP-3 activation was significantly reduced following t

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

10 IGFBP-3 level remained positively associated with T2DM i

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

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

13 IGFBP-3NB administration resulted in a significant decre

14 IGFBP-3NB partially restored VEGF-induced in vivo permea

15 IGFBP-5 is the most conserved IGFBP, and contains 18 cys

16 IGFBPs are composed of cysteine-rich amino- (N-) and car

17 1.16; 95% CI: 1.08-1.24; P(trend) < 0.001), IGFBP-2 (1.18; 1.06-1.31; P(trend) < 0.01) and IGFBP-3 (

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

19 a form of IGFBP-3 that does not bind IGF-1 (IGFBP-3NB), to regulate the blood retinal barrier (BRB)

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

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

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

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

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

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

26 Vimentin, cystatin C, galectin-1, IGFBP-7, and secreted protein, acidic and rich in cystei

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

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

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

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

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

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

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

34 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

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

36 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

37 s (Nix, PUMA) and tumor suppression (GDF-15, IGFBP-6), particularly in cells with high integrin expre

38 nsulin-like growth factor-binding protein 2 (IGFBP-2) is a member of a family of six highly conserved

39 insulinlike growth factor-binding protein 2 (IGFBP-2), nerve growth factor (b-NGF), platelet-derived

40 of insulin growth factor-binding protein-2 (IGFBP-2), which is secreted thereby promoting angiogenes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 nsulin-like growth factor binding protein-4 (IGFBP-4), a well documented inhibitor of the IGF-1/IGF-1

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

59 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:

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

61 rtantly, PHB2 knockdown completely abolished IGFBP-6-mediated RMS cell migration.

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

63 In addition, IGFBP-6 indirectly increases PHB2 tyrosine phosphorylati

64 equires functional cooperation with adjacent IGFBP and TSP1 domains to stimulate MMP-1 expression.

65 helial monolayers (BREC) were measured after IGFBP-3NB treatment.

66 However, by 80 weeks of age IGFBP-3KO mice tended to exhibit larger prostate tumors

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

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

69 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

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

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

72 t IGF-I and its binding proteins IGFBP-1 and IGFBP-2 have potentially beneficial effects on diabetes

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

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

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

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

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

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

79 growth factor binding protein (IGFBP)-2, and IGFBP-6.

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

81 IGF-binding proteins (IGFBP-2, IGFBP-3, and IGFBP-5).

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

83 in contraction-promoting growth factors and IGFBP message levels.

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

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

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

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

88 PHB2 and IGFBP-6 co-localize on the RMS cell surface, and they sp

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

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

91 Both IGFBP-vWC and IGFBP-vWC-TSP1 forms exhibited predictable variations of

92 ol study to investigate circulating IGFs and IGFBPs in PSA-detected prostate cancer with regard to th

93 distinct growth factor signaling pathways as IGFBP-4 inhibited FGF-2- and IGF-1-stimulated angiogenes

94 ributed to loss of growth factor-attenuating IGFBPs, changes in local expression of contraction-promo

95 In sum, the IGF axis, IGFBP-2 in particular, may be implicated in the pathogen

96 was fivefold lower among women with baseline IGFBP-2 levels in the top versus bottom quintile (odds r

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

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

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

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

101 Both IGFBP-vWC and IGFBP-vWC-TSP1 forms exhibited predictable

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

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

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

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

106 IGFBP-5 is the most conserved IGFBP, and contains 18 cysteines, but only 2 of 9 putati

107 a member of a family of six highly conserved IGFBPs that are carriers for the insulin-like growth fac

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

109 In contrast, IGFBP-6-induced MAPK pathway activation was not affected

110 Cq-IGFBP is the first IGFBP family member shown to specific

111 d on bioinformatics analyses, the deduced Cq-IGFBP was shown to share high sequence homology with IGF

112 Recombinant Cq-IGFBP (rCq-IGFBP) protein was produced and, using a "pul

113 wth factor-binding protein (IGFBP) termed Cq-IGFBP.

114 y on prostate cancer development, we crossed IGFBP-3KO mice with a c-Myc-driven model of CaP that dev

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

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

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

118 indicate that the three N-terminal domains (IGFBP, VWC, and TSP1), but not the C-terminal CT domain,

119 splenic lymphomas occurred in 23% of female IGFBP-3KO mice by 80 weeks of age.

120 Cq-IGFBP is the first IGFBP family member shown to specifically interact with

121 n a GCGCCXXC motif that is conserved in five IGFBPs.

122 (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

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

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

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

126 g affinities for PHB2 are 9.0 +/- 1.0 nM for IGFBP-6 and 10.2 +/- 0.5 nM for mIGFBP-6, a non-IGF-bind

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

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

129 We synthesized a HBD peptide specific for IGFBP-2 and demonstrated in vitro that it rescued the mi

130 Cell lines established from IGFBP-3KO:Myc tumors displayed more aggressive phenotype

131 Analysis of aortas obtained from IGFBP-2(-/-) mice showed that RPTPbeta was activated, an

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

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

134 In contrast, higher IGFBP-2 levels were related to a substantially lower ris

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

136 important implications for understanding how IGFBPs modulate the cellular response to IGF-I.

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

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

139 ectiveness of IGF1/IGF binding protein (IGF1/IGFBP) complex dissociation using sodium dodecyl sulfate

140 and cross-sectional insulin, IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in the Boyd Orr cohort (n = 182 men,

141 ally important roles for circulating IGF-II, IGFBP-2, and IGFBP-3 in PSA-detected prostate cancer, in

142 d measurements of blood serum IGF-I, IGF-II, IGFBP-2, and IGFBP-3 obtained at recruitment.

143 ave definitively mapped 5 disulfide bonds in IGFBP-5.

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

145 ontaneous prostate tumors did not develop in IGFBP-3KO mice, but splenic lymphomas occurred in 23% of

146 In Boyd Orr, a one SD increase in IGFBP-2 was associated with 2.6% slower get-up and go ti

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

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

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

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

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

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

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

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

155 Intact IGFBP-3 attenuated extracellular matrix contraction in r

156 Intact IGFBP-3 modulates Muller cell tractional force generatio

157 Unlike their ILP ligands, IGFBPs are highly conserved across evolution, from ancie

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

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

160 Prostates in IGFBP-3 knockout mice (IGFBP-3KO mice) failed to undergo apoptosis after castra

161 In addition, Myc:IGFBP-3KO cells exhibited evidence of epithelial-mesench

162 a key role in this IGF-independent action of IGFBP-6 and suggest a possible therapeutic target for RM

163 f these IGF-independent migratory actions of IGFBP-6 are largely unknown.

164 ges were rescued following administration of IGFBP-2.

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

166 Intravitreal administration of IGFBP-3NB preserves junctional integrity in the presence

167 hibition of PAPP-A and increased cleavage of IGFBP-4 in vitro, resulting in higher bioavailability of

168 tly (Ki = 68 pm) inhibits PAPP-A cleavage of IGFBP-4, and we show in a cell-based assay that STC1 eff

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

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

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

172 The C-domain but not the N-domain of IGFBP-6 is involved in PHB2 binding.

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

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

175 vity restored the anti-angiogenic effects of IGFBP-4 on VEGF-induced blood vessel growth in vivo.

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

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

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

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

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

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

182 In vivo, intravitreal injection of IGFBP-3NB reduced vascular leakage associated with intra

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

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

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

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

187 s not only establish a disulfide bond map of IGFBP-5 but also define a general approach that takes ad

188 nM for mIGFBP-6, a non-IGF-binding mutant of IGFBP-6.

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

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

191 We conclude that the HBD peptide of IGFBP-2 has anabolic activity by activating IGF-I/Akt an

192 were performed without chemical reduction of IGFBP-5.

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

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

195 novel mechanism for coordinate regulation of IGFBP-2 and IGF-I signaling functions that lead to stimu

196 Cs and that endoglin-dependent regulation of IGFBP-4 secretion was crucial for stromal cell-condition

197 span membrane protein, is a key regulator of IGFBP-6-induced RMS cell migration.

198 We investigated the role of IGFBP-2 and receptor protein tyrosine phosphatase beta (

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

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

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

202 = 3), IGFBP3 (n = 3), acid-labile subunit of IGFBP (IGFALS; n = 2), IGF1 receptor (IGF1R; n = 4), and

203 ans may similarly result in the secretion of IGFBPs, with important ramifications for diseases associ

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

205 s, ternary complex formation with IGFBP-3 or IGFBP-5 and the auxillary protein, acid labile subunit,

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

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

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

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

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

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

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

213 insulin-like growth factor-binding protein (IGFBP) 1 mRNAs to be downregulated and upregulated, resp

214 insulin-like growth factor-binding protein (IGFBP) and von Willebrand factor type C (vWC) domains.

215 y the insulin growth factor binding protein (IGFBP) homolog ImpL2, an antagonist of insulin signaling

216 insulin-like growth factor-binding protein (IGFBP) termed Cq-IGFBP.

217 insulin-like growth factor binding protein (IGFBP), and carbonic anhydrase-I and -II.

218 Insulin-like growth factor binding protein (IGFBP)-1 influences fetal growth by modifying insulin-li

219 insulin-like growth factor binding protein (IGFBP)-2, and IGFBP-6.

220 Insulin-like growth factor binding protein (IGFBP)-3 regulates cell proliferation and apoptosis in e

221 insulin-like growth factor-binding protein (IGFBP)-4 and hence release within tissues of bioactive I

222 in-like growth factor (IGF)-binding protein (IGFBP)-6 decreases cancer cell proliferation and surviva

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

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

225 rmation about IGFs and IGF-binding proteins (IGFBP) in cancers detected by the prostate-specific anti

226 insulin-like growth factor-binding proteins (IGFBP) in the conditioned medium from endoglin-deficient

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

228 insulin-like growth factor-binding proteins (IGFBPs) are involved in regulating the effects of insuli

229 insulin-like growth factor-binding proteins (IGFBPs) comprise a conserved family of secreted molecule

230 that several secreted IGF-binding proteins (IGFBPs) exist in mammals, our work raises the possibilit

231 IGF binding proteins (IGFBPs) modify IGF-I actions independently of IGF bindin

232 roteolytic cleavage of IGF-binding proteins (IGFBPs).

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

234 d sufficient for in vitro recognition by rCq-IGFBP.

235 Recombinant Cq-IGFBP (rCq-IGFBP) protein was produced and, using a "pulldown" meth

236 tral analysis and an immunological tool, rCq-IGFBP was shown to bind the Cq-IAG prohormone.

237 More recently, IGFBP-6 was found to promote the migration of rhabdomyos

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

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

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

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

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

243 We propose that the tumor-secreted IGFBP creates insulin resistance in distant tissues, thu

244 Serum IGFBP-3 protein concentrations were significantly lower

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

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

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

248 Of the six IGFBPs, IGFBP3 has the greatest interaction with the lar

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

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

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

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

253 In the current study, we postulated that IGFBP-2 increased bone mass partly through the activity

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

255 We report for the first time that IGFBP-4 differentially inhibits angiogenesis induced by

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

257 The IGFBP-vWC form has potent proangiogenic properties promo

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

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

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

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

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

263 ses were observed at this time in 55% of the IGFBP-3KO mice but none in the control animals.

264 arization, whereas ectopic expression of the IGFBP-vWC variant exacerbated pathological angiogenesis.

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

266 us-mediated expression of either CCN1 or the IGFBP-vWC-TSP1 form reduced ischemia-induced neovascular

267 form containing completely or partially the IGFBP and vWC domains as a surrogate marker of CCN1 acti

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

269 nal tubular structure formation, whereas the IGFBP-vWC-TSP1 variant suppressed cell growth and angiog

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

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

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

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

274 ident diabetes with baseline levels of three IGFBPs and free IGF-I, consistent with hypotheses that t

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

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

277 hree-module forms comprising, in addition to IGFBP and vWC, the thrombospondin type 1 (TSP1) repeats

278 esistance of VEGF-stimulated angiogenesis to IGFBP-4 inhibition appears to depend on sustained activa

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

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

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

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

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

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

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

286 th increased levels of MIP1gamma, LIX, VCAM, IGFBP-6, and GM-CSF in the bronchoalveolar lavage fluid.

287 influence insulin sensitivity, probably via IGFBP-3.

288 When IGFBP-3NB was applied basally to bovine retinal endothel

289 ratio of IGF-I to IGFBP-3 increased, whereas IGFBP-2 decreased throughout pregnancy.

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

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

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

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

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

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

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

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

298 s shown to share high sequence homology with IGFBP family members from both invertebrates and vertebr

299 y, laser-injured mouse retinas injected with IGFBP-3NB plasmid demonstrated reduced vascular permeabi

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