ライフサイエンスコーパス: IGF-I

1 IGF-I (25 ng/ml) significantly protected VSMCs from beta

2 IGF-I led to activation of both the IGF-IR and IR and pr

3 IGF-I levels were significantly associated with PCa risk

4 IGF-I may be an immunomodulatory candidate because it pr

5 IGF-I protected completely against rapamycin-induced apo

6 IGF-I shares structural homology and in vitro metabolic

7 IGF-I stimulated sustained Src activation, which occurre

8 IGF-I suppressed levels of phospho-Smads 2 and 3 with ki

9 IGF-I thus occupies a critical position in the maintenan

10 IGF-I was strongly expressed by macrophages within injur

11 IGF-I-stimulated downstream signaling and biological act

12 IGF-I-stimulated sarcoma viral oncogene (Src) activation

13 ered levels of insulin-like growth factor 1 (IGF-I) and its binding protein 3 (IGFBP3).

14 in glucose and insulin-like growth factor 1 (IGF-I) levels.

15 both impaired binding to IGF-IR and to SHP-2 IGF-I increased SHPS-1 phosphorylation, SHP-2 associatio

16 on IGF-IR is mimicked by exogenous des-(1-3)IGF-I and is blocked by the IGF-IR inhibitor H1356.

17 ,780 increases the concentration of des-(1-3)IGF-I necessary to activate this cascade, whereas estrog

18 AKT activity and its activation by des-(1-3)IGF-I.

19 rtantly, Treg depletion completely abolished IGF-I-mediated protection confirming the therapeutic pot

20 IGFBP-2 has anabolic activity by activating IGF-I/Akt and beta-catenin signaling pathways.

21 ent overweight or obesity, nor did it affect IGF-I levels at age 11.5 years.

22 d that Nox4 Tyr-491 was phosphorylated after IGF-I stimulation and was responsible for Nox4 binding t

23 Moreover, while nearly all IGF-I-ir neurons expressed GSK3beta, some expressed it m

24 e conducted to determine how p66(shc) alters IGF-I-stimulated Src activation, leading to decreased IG

25 ated Src activation, which in turn amplifies IGF-I-linked downstream signaling and biological actions

26 oids via binding its receptor TMEM219, in an IGF-I-independent manner, and disrupted in vivo CoSC fun

27 ism for coordinate regulation of IGFBP-2 and IGF-I signaling functions that lead to stimulation of VS

28 iated (0.99; 0.91-1.08; P(trend) = 0.62) and IGF-I was inversely associated (0.85; 0.79-0.91; P(trend

29 A-BRF infants had normal HMW adiponectin and IGF-I levels at 4 months, whereas SGA-FOF infants had el

30 high-molecular-weight [HMW] adiponectin and IGF-I) of infants born small for gestational age (SGA).

31 on (by absorptiometry), HMW adiponectin, and IGF-I were assessed at birth and 4 months in BRF infants

32 ate the insulin receptor (IR)-A and IR-B and IGF-I receptor (IGF-IR) in vitro; 2) plasma concentratio

33 so reduces the basal IRS-1 concentration and IGF-I-stimulated IRS-1-linked signaling.

34 2 phagocyte oxidase (p22phox) expression and IGF-I stimulated Nox4/p22phox complex formation, leading

35 HMW adiponectin (particularly SGA-FOF1) and IGF-I (particularly SGA-FOF2).

36 At gestational weeks 10-14, both IGF-I and IGF-I/IGFBP-3 were positively associated with GDM risk;

37 Cav-1 also interacts with insulin and IGF-I receptors (IGF-IR/IR) and can stimulate IR kinase

38 oteins at Ser sites that inhibit insulin and IGF-I signaling.

39 th factor family, which includes insulin and IGF-I.

40 Decorin bound with high affinity IGF-IR and IGF-I at distinct sites and negatively regulated IGF-IR

41 he immunological properties of the liver and IGF-I could be beneficial in the treatment of the diseas

42 dence of a mechanistic link between mTOR and IGF-I signaling, two critical regulators of cell growth

43 ovel mechanism of cross-talk between PRL and IGF-I in breast cancer cells, with implications for our

44 We previously reported that PRL and IGF-I synergize in breast cancer cells to activate ERK1/

45 CH2 domain, a unique domain in p66(shc), and IGF-I stimulates this interaction.

46 ulated NADPH oxidase 4 (Nox4) synthesis, and IGF-I facilitated its recruitment to a signaling complex

47 ed protein kinase (MAPK) pathways as well as IGF-I-induced Akt- and MAPK-dependent phosphorylation of

48 However, in astrocytes, IGF-I retains its protective action against oxidative st

49 oteins of the IGF-IR pathway, and attenuated IGF-I-dependent activation of Akt and MAPK.

50 uingly, PRL co-treatment with IGF-I augments IGF-I receptor (IGF-IR) phosphorylation 2-fold higher th

51 tatistically significant association between IGF-I concentration and FOXO3 (rs2153960, chromosome 6q2

52 ly reduced ability of cleaved IGFBP3 to bind IGF-I or to block IGF-I-induced cell signaling.

53 of cleaved IGFBP3 to bind IGF-I or to block IGF-I-induced cell signaling.

54 At gestational weeks 10-14, both IGF-I and IGF-I/IGFBP-3 were positively associated with

55 sm for decorin in negatively modulating both IGF-I and its receptor.

56 a fully human antibody that neutralizes both IGF-I and IGF-II and inhibits IGF signaling through both

57 ecause it is critical for production of both IGF-I and IGF-II, we ablated glucose-regulated protein 9

58 n of insulin receptor substrate (IRS)-1/2 by IGF-I receptor tyrosine kinase is essential for IGF acti

59 trary, Pyk2, which was strongly activated by IGF-I, was critical for IGF-IR-dependent motility and in

60 indicate that armoring of AKT activation by IGF-I is crucial to preserve its cytoprotective effect i

61 her E-peptide increased IGF-IR activation by IGF-I, and this was achieved through enhanced cell surfa

62 inhibit AKT (protein kinase B) activation by IGF-I, which is in contrast to our previous observations

63 refractory to further promoter activation by IGF-I.

64 Rather, stimulation of AKT by IGF-I was significantly higher and more sustained in ast

65 Stimulation of AKT by IGF-I, mimicked also by a constitutively active AKT muta

66 moted cell growth similar to that induced by IGF-I.

67 signalling and cell proliferation induced by IGF-I.

68 Breast cancer cell proliferation mediated by IGF-I was suppressed by attenuating xCT expression or bl

69 Suppression of BMP4 signaling by IGF-I was reversed by chemical inhibitors of phosphoinos

70 ll tractional force generation stimulated by IGF-I and IGF-II while the effects of the vitreous-type

71 ta support that the induction of Survivin by IGF-I occurs through a transcriptional mechanism that is

72 ORC2 represses the expression of Survivin by IGF-I.

73 fat (inverse), lactose, fiber, and calcium; IGF-I/IGFBP-3 with lactose and calcium; and IGFBP-1 with

74 er, which was abolished in mice with chronic IGF-I deficiency (LID).

75 Circulating IGF-I and IGFBP-3 concentrations predict anthropometric

76 hose of littermate controls, and circulating IGF-I also decreased significantly, yet glucose homeosta

77 , with a 70% to 80% reduction in circulating IGF-I levels, were protected against three of four chemo

78 9 recombinant protein normalized circulating IGF-I/IGFBP3 levels and reestablished CoSC homeostasis.

79 ggesting that reducing levels of circulating IGF-I might not prevent the initiation of prostate cance

80 A 72-hour fast in mice reduced circulating IGF-I by 70% and increased the level of the IGF-I inhibi

81 apy-dependent damage by reducing circulating IGF-I levels and by a mechanism that involves downregula

82 th correlated with birth weight, circulating IGF-I, and total and abdominal fat at age 2 weeks.

83 may be relevant to unveil new ways to combat IGF-I/insulin resistance.

84 mulated Src activation, leading to decreased IGF-I actions.

85 demonstrate that transient, plasmid-derived IGF-I expression in mouse liver suppressed autoimmune di

86 Three different IGF-I isoforms were detected in heifers with Class 1 tra

87 Consistently, PRL diminished IGF-I-induced IGF-IR internalization, which may result f

88 1 thus potentially modulating the downstream IGF-I signal pathway.

89 IGFBP-2 enhanced IGF-I-stimulated VSMC migration and proliferation.

90 nflammatory cytokine production and enhanced IGF-I-stimulated VSMC proliferation.

91 such cleavage is shown to result in enhanced IGF-I-independent ability of cleaved IGFBP3 to block FGF

92 rough promoting Epsin1 binding, and enhances IGF-I receptor-induced IRS-2 tyrosine phosphorylation.

93 he mechanism by which hyperglycemia enhances IGF-I-stimulated Src activation and the role of NADPH ox

94 Low concentrations of EPO+IGF-I provided neuroprotection from gp120 in vitro in a

95 various concentrations of EPO, IGF-I, or EPO+IGF-I from gp120-induced damage in vitro.

96 st that chronic combination therapy with EPO+IGF-I provides neuroprotection in a mouse model of HAND,

97 rain following transnasal treatment with EPO+IGF-I, in addition to neuroprotection we observed increa

98 ve effects of various concentrations of EPO, IGF-I, or EPO+IGF-I from gp120-induced damage in vitro.

99 Permanent protection depended on exogenous IGF-I expression in liver nonparenchymal cells and was a

100 Our results show that following IGF-I stimulation, PDK1 is recruited to SHPS-1, and its

101 ant correlations (P < 0.05) were as follows: IGF-I with total protein, lactose, calcium, and sodium;

102 0.02 standard deviations (-0.12 to 0.08) for IGF-I.

103 e (ORQ4-Q1) was 2.93 (95% CI 1.18, 7.30) for IGF-I and 3.31 (1.10, 9.98) for IGF-I/IGFBP-3.

104 8, 7.30) for IGF-I and 3.31 (1.10, 9.98) for IGF-I/IGFBP-3.

105 n, which markedly increases its affinity for IGF-I, is regulated by mechanistic target of rapamycin (

106 Although our findings for IGF-I agree with previous results from PSA screening tri

107 PDK1 recruitment was also required for IGF-I to prevent apoptosis that occurred in response to

108 S-1 signaling complex, which is required for IGF-I-stimulated AKT Thr(308) phosphorylation and inhibi

109 esponse to hyperglycemia and is required for IGF-I-stimulated Src activation.

110 Grb2-PDK1 complex on SHPS-1 was specific for IGF-I signaling because inhibiting PDK1 recruitment to S

111 ith baseline levels of three IGFBPs and free IGF-I, consistent with hypotheses that the IGF axis migh

112 associated with total IGF-I levels, but free IGF-I and diabetes had a significant association that va

113 for Cnr1 to promote growth, regulate the GH/IGF-I axis, and improve beta-cell function and glucose h

114 There was some evidence that high IGF-I and low insulin levels in middle-age were associat

115 igher IGFBP-3 (P = 4.4 x 10(-21)) and higher IGF-I (P = 4.9 x 10(-9)) concentrations; when the two me

116 Only the higher IGF-I group had significant improvements in immediate ve

117 ese findings suggest that the growth hormone/IGF-I system may be a potential therapeutic target follo

118 the insulin analog AspB10, recombinant human IGF-I, or vehicle.

119 Insulin-like growth factor I (IGF-I) exerts multiple effects on different retinal cell

120 converging on insulin like growth factor I (IGF-I) expression.

121 of insulin or insulin-like growth factor I (IGF-I) in combination with oxygen supplementation were s

122 Insulin-like growth factor I (IGF-I) is a mitogen for vascular smooth muscle cells (VS

123 Serum insulin-like growth factor I (IGF-I) levels consistently increased after one dose of c

124 centrations of insulin-like growth factor I (IGF-I) or the bioavailability of estradiol.

125 Insulin and insulin-like growth factor I (IGF-I) signal through the scaffold protein insulin recep

126 Disruption of insulin-like growth factor I (IGF-I) signaling is a key step in the development of can

127 y to decreased insulin-like growth factor I (IGF-I) signaling, a pathway also implicated in aging.

128 tripeptide of insulin-like growth factor I (IGF-I) treatment.

129 ed to insulin, insulin-like growth factor I (IGF-I), and leptin.

130 ctin (PRL) and insulin-like growth factor I (IGF-I), both of which have also been implicated in breas

131 promoter region of insulin growth factor I (IGF-I), fibroblast growth factor 10 (FGF-10), and Epithe

132 r by affecting insulin-like growth factor I (IGF-I)-mediated mitogenesis.

133 Insulin-like growth factor-I (IGF-I) and insulin-like growth factor-binding protein-3

134 h hormone (GH)-insulin-like growth factor-I (IGF-I) axis regulates somatic growth during childhood an

135 h by modifying insulin-like growth factor-I (IGF-I) bioavailability.

136 Circulating insulin-like growth factor-I (IGF-I) has been studied extensively in prostate cancer,

137 Insulin-like growth factor-I (IGF-I) is an essential growth factor that regulates the

138 of circulating insulin-like growth factor-I (IGF-I) levels [OR(per allele) = 1.46 (95% CI, 1.04-2.06)

139 ery, and serum insulin-like growth factor-I (IGF-I) may mediate this effect.

140 etin (EPO) and insulin-like growth factor-I (IGF-I) protects against HIV/gp120-mediated neuronal dama

141 O4, an insulin/insulin-like growth factor-I (IGF-I) responsive transcription factor associated with l

142 ivation of the insulin-like growth factor-I (IGF-I) signaling has been implicated in the development

143 ivation of the insulin-like growth factor-I (IGF-I) signaling pathway, implicated in the development

144 ose respond to insulin-like growth factor-I (IGF-I) with increased protein synthesis but do not proli

145 erglycemia and insulin-like growth factor-I (IGF-I), SHPS-1 functions as a scaffold protein, and a si

146 al population, insulin-like growth factor-I (IGF-I)-enhanced cell cycle entry by >5-fold compared wit

147 ied, including insulin-like growth factor-I (IGF-I).

148 Insulin-like growth factors (IGF), IGF-I and IGF-II, are small polypeptides involved in reg

149 There is growing evidence that the impaired IGF-I system contributes to neurodegeneration.

150 1 recruitment to SHPS-1, leading to impaired IGF-I-stimulated AKT Thr(308) phosphorylation.

151 variant in rabbits resulted in a 14% fall in IGF-I over 7 days.

152 S that a standard deviation (SD) increase in IGF-I was associated with 1.5% faster get-up and go test

153 ox4-derived reactive oxygen species (ROS) in IGF-I-stimulated Src activation was investigated via kno

154 e in response to IGF-I and display increased IGF-I gene expression and protein synthesis.

155 scription factor C/EBPdelta which can induce IGF-I in response to PGE2, but conversely prevented the

156 The IGF1R antibody dalotuzumab inhibited IGF-I-mediated Akt phosphorylation, proliferation, and a

157 qual potency for the IGF1R and IR, inhibited IGF-I-, IGF-II-, and insulin-stimulated Akt phosphorylat

158 SHPS-1 in aorta from diabetic mice inhibited IGF-I-stimulated Src oxidation and activation as well as

159 xamined prospective associations of insulin, IGF-I, IGF-II and IGFBP-3 with physical performance in t

160 ; n = 739 men); and cross-sectional insulin, IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in the Boyd Orr cohor

161 Finally, an insulin/IGF-I gene expression signature predicted recurrence-fre

162 Inhibition of placental mTOR and insulin/IGF-I signaling resulting in down-regulation of placenta

163 istic target of rapamycin (mTOR) and insulin/IGF-I signaling, down-regulates placental nutrient trans

164 signaling in isolated rat islets by insulin/IGF-I (used as an experimental in vitro tool) or downstr

165 Abnormalities in insulin/IGF-I signaling activate muscle protein degradation in t

166 phorylation of proteins in the mTOR, insulin/IGF-I, ERK1/2, and GSK-3 signaling pathways in placental

167 ect may be mediated by inhibition of insulin/IGF-I and mTOR signalling pathways, which are positive r

168 ypes (e.g. GHRH/ghrelin/somatostatin/insulin/IGF-I-receptors/Pit-1).

169 hat, when chronically increased, intraocular IGF-I is responsible for the induction of deleterious ce

170 s hyperinsulinemia and insulin receptor (IR)/IGF-I receptor (IGF-IR) phosphorylation in tumors are as

171 NULL/Y) mice were treated with a full-length IGF-I modified with the addition of polyethylene glycol

172 argine (GLA), metabolites 1 (M1) and 2 (M2), IGF-I, and NPH insulin to activate the insulin receptor

173 The Igf1 gene encodes mature IGF-I and a carboxy-terminal extension called the E-pept

174 IGF binding proteins (IGFBPs) modify IGF-I actions independently of IGF binding, but a recept

175 ty, but instead affect growth via modulating IGF-I signaling, thereby increasing the complexity of IG

176 the Igf-1 gene are complex yielding multiple IGF-I transcript isoforms with putative functional contr

177 Murine IGF-I transcript expression was more diverse utilizing m

178 us, unlike liver production of IGF-I, muscle IGF-I is necessary not only locally but also globally fo

179 regulation of IGF-IR and its ligands, namely IGF-I and IGF-II.

180 f IGF-II occur via IGF-II receptors, and not IGF-I receptors, and target both basal and learning-depe

181 (1.27; 1.19-1.36; P(trend) < 0.001), but not IGF-I (0.99; 0.93-1.04; P(trend) = 0.62), were associate

182 lls proliferate in response to PDGF, but not IGF-I or IGF-II.

183 osylation of the IGFR disrupt the ability of IGF-I to protect against the osteogenic differentiation

184 R), which mediates the biological actions of IGF-I and IGF-II, has emerged in recent years as a promi

185 n is also required for maximal activation of IGF-I signalling and cell proliferation in prostate canc

186 Thus, the clinical benefit of IGF-I treatment in RTT may critically depend on the dose

187 we show that MEDI-573 blocks the binding of IGF-I and IGF-II to IGF-1R or IR-A, leading to the inhib

188 naling, thereby increasing the complexity of IGF-I biological activity.

189 t vary with either the amount or duration of IGF-I treatment.

190 markedly attenuated the inhibitory effect of IGF-I on beta-glycerophosphate-induced mineralization (p

191 ignificantly inhibited the in vivo growth of IGF-I- or IGF-II-driven tumors.

192 proliferation and migration independently of IGF-I and its receptor (IGF-IR), but the mechanism by wh

193 e results demonstrate that the inhibition of IGF-I and IGF-II ligands by MEDI-573 results in potent a

194 Hypoxic inhibition of IGF-I and Runx2 were enforced by glucocorticoid, and con

195 , and this was associated with inhibition of IGF-I stimulated AKT Ser473 phosphorylation and VSMC pro

196 A single injection of IGF-I, but not PBS, into injured muscle to replace IGF-I

197 (-) macrophages, and produce a high level of IGF-I to promote muscle regeneration.

198 ic mice with increased intraocular levels of IGF-I showed progressive impairment of electroretinograp

199 , that is, a significant increased number of IGF-I expressing neurons versus a reduced number of IGFB

200 variable analyses, significant predictors of IGF-I were energy (beta = 0.14, P < 0.05) and calcium (b

201 Thus, unlike liver production of IGF-I, muscle IGF-I is necessary not only locally but al

202 (IGFBP-3) concentrations and molar ratio of IGF-I to IGFBP-3 increased, whereas IGFBP-2 decreased th

203 Restoration of IGF-I was sufficient to reverse the protective effect of

204 ency in the liver to investigate the role of IGF-I in regulating the host microenvironment and colore

205 we offer evidence that a critical support of IGF-I in prostate cancer is mediated by its ability to s

206 for the enhancing effect of hyperglycemia on IGF-I-stimulated Src activation, which in turn amplifies

207 prevented the stimulatory effect of PGE2 on IGF-I mRNA.

208 s much more modest changes in glucose and/or IGF-I levels, and promotes chronic weight loss in both r

209 n Mecp2(NULL/Y) mice; however, high-dose PEG-IGF-I decreased lifespan.

210 Low-dose PEG-IGF-I treatment slightly improved lifespan and heart rat

211 ith the addition of polyethylene glycol (PEG-IGF-I), which improves pharmacological properties.

212 her insulinotropic off-target effects of PEG-IGF-I caused the detrimental effect, we treated Mecp2(NU

213 These findings demonstrate that peripheral IGF-I/IGFBP3 controls CoSCs and their dysfunction in DE.

214 Plasma IGF-I and IGF binding protein 3 (IGFBP-3) concentrations

215 For example, interference of the prosurvival IGF-I/AKT/FOXO3 pathway by redox activation of the stres

216 at5 sequences in 200 kb centering on the rat IGF-I gene, 22 resided within conserved regions and/or w

217 omplemented on administration of recombinant IGF-I.

218 and interacts with glucocorticoid to reduce IGF-I expression by osteoblasts.

219 with similar levels of adiposity and reduced IGF-I levels without alterations of growth hormone (GH)

220 The pituitary reduced IGF-I expression post-pubertally whereas the uterus incr

221 Reducing IGF-I/IGF-I signaling protected primary glia, but not gl

222 ated chromosomal enhancers that can regulate IGF-I gene transcription.

223 ependent motility and invasion and regulated IGF-I-dependent activation of the Akt and MAPK pathways.

224 ne phosphatase beta (RPTPbeta) in regulating IGF-I signaling and cellular proliferation.

225 but not PBS, into injured muscle to replace IGF-I remarkably improved muscle regeneration in Ccr2(-/

226 mediated small hairpin RNA (shRNA) represses IGF-I-stimulated cell growth, implicating Survivin as a

227 These effects require IGF-I-induced Akt- and MAPK-dependent activation of paxi

228 expression, pituitary GH content, and serum IGF-I levels; and exhibited reduced body size and weight

229 fiber, calcium, zinc, and sodium] and serum IGF-I, IGF binding protein 1 (IGFBP-1), IGF binding prot

230 y to determine the effects of baseline serum IGF-I concentrations on WM tract and neuropsychological

231 state biopsy and measurements of blood serum IGF-I, IGF-II, IGFBP-2, and IGFBP-3 obtained at recruitm

232 I were greater in patients with higher serum IGF-I at baseline.

233 in SPCC FA over time in patients with serum IGF-I above versus below the median for age.

234 Similarly, IGF-I suppressed BMP4-induced transcription of the Id1,

235 ains could mediate GH- and Stat5b-stimulated IGF-I promoter activity in cultured cells.

236 (IGF-IR) phosphorylation 2-fold higher than IGF-I alone.

237 er xenograft models with demonstrations that IGF-I receptor stimulation was sufficient to generate a

238 Here, we offer evidence that IGF-I reduction mediates part of the starvation-dependen

239 We hypothesised that IGF-I and IGF-II are associated with improved, and insul

240 Results indicate that IGF-I signaling to Bad requires activation of PI3K and P

241 s offered in vivo support for our model that IGF-I-mediated activation of mTOR suppresses phosphoryla

242 Our studies thus reveal that IGF-I expression is stratified by two critical transcrip

243 In this study, we show that IGF-I regulates cystine uptake and cellular redox status

244 rostate cell line as a model, we showed that IGF-I induces Survivin expression, and that silencing Su

245 Laboratory models suggest that IGF-I and its binding proteins IGFBP-1 and IGFBP-2 have

246 Taken together, these results suggest that IGF-I signaling through a PI3K/Akt/mTORC1 mechanism elev

247 Collectively, these data suggest that IGF-I-induced phosphorylation of Bad at multiple sites v

248 phase response, and gliosis, suggesting that IGF-I altered normal retinal homeostasis.

249 The IGF-I receptor (IGF-IR), which mediates the biological a

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

251 surements were adjusted for one another, the IGF-I association was attenuated but the IGFBP-3 associa

252 Under these conditions, the IGF-I receptor signals through an alternate scaffold pro

253 activate an upstream response element in the IGF-I gene promoter.

254 ta), as one major downstream molecule in the IGF-I signaling.

255 the intense total GSK3beta expression in the IGF-I-ir neurons belongs to the active form of GSK3beta

256 IGF-I by 70% and increased the level of the IGF-I inhibitor IGFBP-1 by 11-fold.

257 e suggest that the altered expression of the IGF-I system including GSK3beta in spinal cord neurons m

258 e sclerosis, to see if the expression of the IGF-I system is altered.

259 mined for the immunoreactivities (ir) of the IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synt

260 in the non EAE spinal cords did not show the IGF-I immunoreactivity, they were numerously positive fo

261 format and established that all bind to the IGF-I receptor and both insulin receptors A and B, resul

262 d to Stat5b binding domains found within the IGF-I transcription unit.

263 f the Survivin promoter are involved in this IGF-I response.

264 Thus, IGF-I promoted the proliferation of ER(+) breast cancer

265 Thus, our findings pointed to IGF-I receptor stimulation as a rational strategy to suc

266 associations were only partially related to IGF-I and leptin.

267 ulin receptor (IR), and failed to respond to IGF-I-induced Akt activation, proliferation, and anchora

268 omyoma (UL) cells proliferate in response to IGF-I and display increased IGF-I gene expression and pr

269 racellular matrix contraction in response to IGF-I and IGF-II while the IGFBP-3 fragment modulated ce

270 enhanced Akt phosphorylation in response to IGF-I and increased beta-catenin signaling through two m

271 erequisite for its activation in response to IGF-I during hyperglycemia.

272 in receptor isoform A (IR-A), in response to IGF-I receptor (IGF-IR) inhibition and perturbations in

273 racellular matrix contraction in response to IGF-I, IGF-II, and PDGF.

274 e PTEN at the plasma membrane in response to IGF-I, inducing its cytosolic translocation and preservi

275 idation and activation of Src in response to IGF-I, whereas knockdown of Nox1 had no effect.

276 how IGFBPs modulate the cellular response to IGF-I.

277 ation, and cell proliferation in response to IGF-I.

278 ress that results in an enhanced response to IGF-I.

279 Src homology 3 domain in Grb2 in response to IGF-I.

280 he cell cycle exhibited similar responses to IGF-I in terms of integrated Akt activity and migration

281 cular smooth muscle cell (VSMC) responses to IGF-I, we overexpressed IRS-1 in VSMCs maintained in hig

282 dedifferentiation and enhances responses to IGF-I.

283 rast, hyperglycemia alters responsiveness to IGF-I, resulting in increased SHPS-1 phosphorylation and

284 The mice showed enhanced sensitivity to IGF-I stimulation of VSMC proliferation and a hyperproli

285 vation, thereby altering VSMC sensitivity to IGF-I.

286 Diabetes was not associated with total IGF-I levels, but free IGF-I and diabetes had a signific

287 Tumor IGF-I receptor expression by immunohistochemistry did no

288 Upon IGF-I stimulation, pVHL-deficient RCC cells exhibit incr

289 ed inhibition of migration and invasion upon IGF-I stimulation.

290 ce, IGF-II, via IGF-II receptor, but not via IGF-I receptor, reverses the abnormal levels of the AMPK

291 metabolic syndrome and investigated whether IGF-I treatment might improve this phenotype.

292 IGF-II and prepared six IGF-II analogs with IGF-I-like mutations.

293 wever, a novel IGF1 SNP, not associated with IGF-I blood levels, shows preliminary evidence for assoc

294 iomarkers-particularly elevated calcium with IGF-I and IGFBP-3 and elevated vegetable protein with IG

295 GFBP-3 fragment alone or in combination with IGF-I or IGF-II.

296 pVHL competes with IGF-I receptor (IGF-IR) for binding to RACK1 thus potent

297 t rather that it functions coordinately with IGF-I to stimulate growth and skeletal acquisition.

298 with the opposite direction of effect, with IGF-I concentration after adjustment for IGFBP-3 concent

299 At maximal induction with IGF-I, net tissue proliferation increased 3- to 4-fold i

300 Intriguingly, PRL co-treatment with IGF-I augments IGF-I receptor (IGF-IR) phosphorylation 2