ライフサイエンスコーパス: IGF

1 IGF actions are mediated by transmembrane receptors and

2 IGF signaling plays an important role in aging and CR ef

3 IGF-1 also induced expression of the redox regulator nuc

4 IGF-1 rhythms are disrupted in Cry-deficient mice, and I

5 IGF-1-mediated increases in myotube diameter (1.27 +/- 0

6 IGFs have been reported to play a role in asthma, but li

7 Human insulin-like growth factor 1 (IGF-1) is a 70 amino acid protein hormone, with key impa

8 Insulin-like Growth Factor 1 (IGF-1) is associated with cardiovascular disease, itself

9 Insulin-like growth factor 1 (IGF-1) is known to have diverse effects on brain structu

10 y, the insulin/insulin-like growth factor 1 (IGF-1) signaling pathway, mechanistic target of rapamyci

11 could be rescued by insulin growth factor 1 (IGF-1), a drug that is currently in clinical trials for

12 cose, insulin, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein 3 (IG

13 lished that an insulin-like growth factor 1 (IGF-1)-inducible mitochondrial UTP carrier (PNC1/SLC25A3

14 of insulin and insulin-like growth factor 1 (IGF-1).

15 expression of insulin-like growth factor 1 (IGF-1).

16 also contains insulin-like growth factor-1 (IGF-1) and its associated binding proteins, although the

17 or-A (VEGF-A), insulin-like growth factor-1 (IGF-1) and Klotho, in the blood and brain of normal rats

18 x hormones and insulin-like growth factor-1 (IGF-1) in animals.

19 Activation of insulin-like growth factor-1 (IGF-1) receptor (IGF1R) signaling induces keratinocyte m

20 retreated with insulin-like growth factor-1 (IGF-1) showed resolution of the same amount of initial D

21 e polypeptide, insulin-like growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signa

22 unger participants (aged 50-60 y, n = 1400), IGF-1 was associated with lower odds of hearing impairme

23 estradiol on insulin-growth factor-1 and -2 (IGF-1, -2) signaling and metabolic function in primary c

24 ike growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signaling and improves cardia

25 deficient mice exhibit constitutively active IGF signaling, presenting with proinflammatory and immun

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

27 CRC models and the efficacy of MEDI-573, an IGF-1/2-neutralizing antibody.

28 tored with co-treatment of either HDIs or an IGF-1R inhibitor, in combination with TKIs (Figure 5A-B)

29 , MCF-7 cells with acquired resistance to an IGF-1 receptor (IGF-1R) tyrosine kinase inhibitor exhibi

30 Here we report that IGF-1 level in blood and IGF-1 signaling demonstrates circadian rhythms.

31 bitors is associated with increased CD20 and IGF-1 transcript levels in tumors and IGF-1 expression i

32 oxorubicin (DXR) and growth factors (EGF and IGF-1).

33 Y333 in response to stromal signals HGF and IGF-1, respectively, and IGF-1 expression was regulated

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

35 analyzed for leptin, adiponectin, IGF1, and IGF binding protein 3.

36 h PKA-mediated relief of IRS1 inhibition and IGF-1R-dependent tyrosine phosphorylation of IRS1.

37 hy, as corroborated by increased insulin and IGF-1 plasma concentrations in multiple system atrophy p

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

39 egree of homology, insulin receptor (IR) and IGF-1 receptor (IGF1R) mediate distinct cellular and phy

40 expression divergence comparing IGF-IRa and IGF-IRb genes.

41 hms are disrupted in Cry-deficient mice, and IGF-1 level is reduced by 80% in these mice, which leads

42 glucose, inhibit keratinocyte migration and IGF-1-induced chemotaxis in association with inhibition

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

44 naptic growth factors such as BDNF, NGF, and IGF.

45 between ribosomal RNA (rRNA) production and IGF-1-mediated myotube hypertrophy in vitro Primary skel

46 IMP2's ability to promote proliferation and IGF action requires IMP2 phosphorylation by mTOR.

47 mal signals HGF and IGF-1, respectively, and IGF-1 expression was regulated by the Sonic Hedgehog (Sh

48 Src and IGF-1R phosphorylated the prometastatic molecule Annexin

49 20 and IGF-1 transcript levels in tumors and IGF-1 expression in tumor-associated B cells.

50 alling, protecting cancer cells against anti-IGF-1R therapy.

51 ich could be developed into a practical anti-IGF-1R strategy for cancer therapy.

52 yrosine residues 60, 133, and 250 in PCNA as IGF-1R targets, and PCNA phosphorylation was followed by

53 produce a variety of growth factors, such as IGF-1, VEGF-alpha, TGF-beta, and Wnt proteins that regul

54 ha as a potent water-soluble indirubin-based IGF-1R inhibitor.

55 However, the link between IGF-1 and the occurrence of hearing impairment is untest

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

57 but not IRS-1-mediated activation of AKT by IGF-1.

58 e uptake by epithelial cells was enhanced by IGF-1 and led to decreased inflammatory responses by epi

59 way of fibrosis and opacity was inhibited by IGF-1, and further with SAHA in particular, and with hal

60 ions on extrahepatic tissues are mediated by IGF-1.

61 by transmembrane receptors and modulated by IGF-binding proteins.

62 The effects of the FMD are reversed by IGF-1 treatment and recapitulated by PKA and mTOR inhibi

63 In MCF-7 and ZR75.1 breast cancer cells, IGF-1 induces peroxisome proliferator-activated receptor

64 In aggregate, these data identify central IGF-1R as a mediator of the integration of nutrient and

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

66 In the full cohort, IGF-1 was not associated with subsequent hearing impairm

67 alogues, but expression divergence comparing IGF-IRa and IGF-IRb genes.

68 he two beta-arrestin isoforms in controlling IGF-1R expression and function, which could be developed

69 A and suggest that miR-195 and CUGBP1 dampen IGF signaling by inhibiting IGF2R translation.

70 -type HNPCs, RIT1 (-/-) HNPCs show deficient IGF-1-dependent Akt signaling and neuronal differentiati

71 B-cell-derived IGF-1 is critical for resistance of melanomas to BRAF an

72 mediated by tumor-associated B cells-derived IGF-1.

73 t exogenous DHEA significantly downregulated IGF-1 and its receptor in both HCFs and HKCs with HKCs s

74 Suppression of rRNA synthesis during IGF-1 treatment did not prevent early increases in AKT (

75 lopmental transcriptional regulation of each IGF-IR gene, revealing tight co-expression between the I

76 wth hormone (GH) and its downstream effector IGF-1 increase and play critical roles in bone acquisiti

77 Elevated IGF-1/insulin-like growth factor-1 receptor (IGF-1R) aut

78 eptor tyrosine kinases (RTKs) from the ErbB, IGF-1R and Met families in breast cancer cells.

79 r alterations in the coding regions of every IGF family gene, but the vast majority of predicted chan

80 Unlike in cells expressing IGF-1R, externally induced DNA damage in IGF-1R-negative

81 trating B cells to produce the growth factor IGF-1.

82 role of TEC-expressed insulin growth factor (IGF) binding protein-7 (IGFBP7/angiomodulin).

83 Lowered insulin/insulin-like growth factor (IGF) signaling (IIS) can extend healthy lifespan in worm

84 ins, the insulin/insulin-like growth factor (IGF) signaling (IIS) pathway, and the mechanistic target

85 The insulin/insulin-like growth factor (IGF) signaling pathway plays a critical role in the regu

86 Insulin-like growth factor (IGF) signaling plays an important role in cell growth an

87 of mutations in insulin-like growth factor (IGF) signalling genes in 8/112 (7%) of cases.

88 , P < 0.005) and insulin-like growth factor (IGF)-1 (r(2) = 0.80, P < 0.0001) were positively associa

89 egulation of the insulin-like growth factor (IGF)/insulin (IIS)-PI3K-AKT-TOR signaling pathway is lin

90 the role of the insulin-like growth factors (IGFs) in controlling placental resource allocation to fe

91 rogenesis is significantly blunted following IGF-1 infusion in knockout (RIT1 (-/-) ) mice.

92 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.

93 8, 7.30) for IGF-I and 3.31 (1.10, 9.98) for IGF-I/IGFBP-3.

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

95 it does not appear to be a prerequisite for IGF-1-induced myotube hypertrophy in vitro.

96 omal biogenesis response is not required for IGF-1-mediated hypertrophy of human primary myotubes.

97 dies, molecular evidence suggests a role for IGF-1 in hearing function.

98 = 18; SGF, n = 34; immediate graft function [IGF], n = 24).

99 In contrast, genetic IGF-1R dosage was effective only in females, where it al

100 wth hormone-insulin-like growth factor-1 (GH-IGF-1) axis.

101 MP-GHRKO) mice to address the role of the GH/IGF axis in osteocytes.

102 that a subset of CRC cell lines express high IGF-2 levels owing to an increased DNA copy number and h

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

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

105 tro and skin explants ex vivo to examine how IGF-1R activation status affects ATR-CHK1 kinase signali

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

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

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

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

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

111 or the immunoreactivities (ir) of the IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase ki

112 uded demonstrating the effectiveness of IGF1/IGF binding protein (IGF1/IGFBP) complex dissociation us

113 We show the STAT3-mediated IGF2/IGF-1R signaling cascade as a key modulator for both acq

114 e polypeptide insulin-like growth factor II (IGF-II) reverses all these deficits.

115 nistration of insulin-like growth factor II (IGF-II), a polypeptide that crosses the blood-brain barr

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

117 content (-16 +/- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.

118 that mutagenesis and skin carcinogenesis in IGF-1-deficient geriatric skin may be caused by defects

119 Prolactin caused no significant change in IGF-1 levels and an increase in IGF-2 in HKCs correlatin

120 ing IGF-1R, externally induced DNA damage in IGF-1R-negative cells caused G1 cell cycle arrest and S

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

122 nt change in IGF-1 levels and an increase in IGF-2 in HKCs correlating with an increase in ATP and NA

123 vides the mechanism for circadian rhythms in IGF signaling in vivo.

124 lated GTPase, RIT1, plays a critical role in IGF-1-dependent neurogenesis.

125 equences (Arg36 and Arg37), was tolerated in IGF-1R binding and its activation.

126 rtially attenuated in cells with an inactive IGF-1R.

127 inhibitor NT157 has the potential to inhibit IGF-1R and STAT3 signaling pathways in cancer cells and

128 Moreover, we found that citrate inhibited IGF-1R phosphorylation.

129 rowth factor binding protein IGFBP7 inhibits IGF signaling by binding the IGF1 receptor (IGF1R), func

130 pathways but together with the DAF-2/insulin IGF-1 receptor (IIR) signaling pathway to promote germli

131 abditis elegans and long-lived daf-2/insulin/IGF-1 and glp-1/Notch mutants throughout adulthood.

132 d insulin resistance (i.e. decreased insulin/IGF-1) have been reported in other neurodegenerative dis

133 mutations within the growth-hormone, insulin/IGF-1 or mTOR signalling pathways.

134 sing evidence also suggests impaired insulin/IGF-1 signalling in multiple system atrophy, as corrobor

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

136 oxia-inducible factor hif-1, and the insulin/IGF-1 pathway components daf-2, age-1, and daf-16 all al

137 ffects in regulating proteins in the insulin/IGF-1 signaling cascade in vivo in physiological states

138 The insulin/IGF-1 signalling (IIS) pathway plays an important role i

139 assessed by PERCIST 1.0 as early as 9 d into IGF-1R antibody therapy in patients with ESFT can predic

140 Intriguingly, IGF-1 induced beta-catenin and PKM2 expression and enhan

141 (lymphocyte, alpha-linoleic acid metabolism, IGF regulation) including eleven genes as optimal marker

142 In BTBR mice, IGF-II, via IGF-II receptor, but not via IGF-I receptor,

143 MEDI-573 efficiently neutralized IGF-2 and induced apoptosis, which resulted in significa

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

145 rther studies have demonstrated that nuclear IGF-1R (nIGF-1R) physically and functionally interacts w

146 This study reveals contrasting abilities of IGF-1R to interact with each beta-arrestin isoform, depe

147 Absence of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCN

148 HMGA1 suppresses the abundance of IGF binding protein 2/IGFBP2 and Grb14, inhibitors of IG

149 Activation of IGF signaling is a major oncogenic event in diverse canc

150 ot peripheral, pharmacological activation of IGF-1R prevented hypothermia during calorie restriction.

151 Full blockade of IGF-1R affected female and male mice similarly.

152 Moreover, blockade of IGF-2 by MEDI-573 modulated other signaling pathways, su

153 We investigated serum concentrations of IGF-1 and IGFBP-3 and their molar ratio in relation to T

154 We find that disruption of IGF-1R signaling with small-molecule inhibitors or IGF-1

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

156 ular mechanism for the therapeutic effect of IGF-1.

157 a and PRC with siRNA reverses the effects of IGF-1 and disrupts mitochondrial morphology and membrane

158 atherogenesis, but the potential effects of IGF-1 on their function are unknown.

159 The effects of IGF-II occur via IGF-II receptors, and not IGF-I recepto

160 in neonatal mice with impaired expression of IGF-1 and IGFBP3.

161 The mechanism by which expression of IGF-1R is increased in renal carcinoma is not known.

162 The importance of IGF actions in human physiology is strengthened by the r

163 The physiological and clinical importance of IGF-1 prompted challenging chemical and biological trial

164 d overall insulin resistance, independent of IGF-1.

165 n affect cellular functions independently of IGF binding through an Arg-Gly-Asp (RGD) integrin-bindin

166 Furthermore, inhibition of IGF-1R abolished the protection conferred by miR-223 def

167 Pharmacological or genetic inhibition of IGF-1R enhanced the reduction of temperature and of ener

168 ab, a human monoclonal antibody inhibitor of IGF-IR, in patients with active, moderate-to-severe opht

169 ng protein 2/IGFBP2 and Grb14, inhibitors of IGF action.

170 Experiments using several inhibitors of IGF-1 receptor signaling revealed that inhibiting the Ra

171 W541, dasatinib or crizotinib (inhibitors of IGF-1R, Src and c-Met/ALK, respectively) led to synergis

172 portunities to understand the intricacies of IGF signaling and action in both physiological and patho

173 owth factor alpha genes, and a high level of IGF-1 and osteopontin genes compared to mdx(5cv) control

174 observational evidence that higher levels of IGF-1 appeared to confer some protection against hearing

175 nal Study of Ageing provided serum levels of IGF-1 in 2008 and again in 2012.

176 Monocytes/macrophages express high levels of IGF-1 receptor (IGF1R) and play a pivotal role in athero

177 CRC mouse models that express high levels of IGF-2.

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

179 , we investigated the oncogenic potential of IGF-2 in IGF2-overexpressing CRC models and the efficacy

180 d a statistically significantly reduction of IGF-1 in CRvs.AL by 50 to 70% in WT mice at several dail

181 Down-regulation of IGF-1 upon Cry deficiency correlates with reduced Igf-1

182 The reported immune-responsive regulation of IGF-IR genes adds to an emerging body of evidence that s

183 aken together, our results suggest a role of IGF-1R in DDT.

184 Suppression of IGF binding protein-3 by palmitate promotes hepatic infl

185 Lifespan extension via the suppression of IGF-1/insulin-like signaling (IIS) offers a possibility

186 w method for the total chemical synthesis of IGF-1 analogs, which entails the solid-phase synthesis o

187 Targeting of IGF-1 and PI3K(p85alpha) by miR-29b is required for indu

188 ple types of muscle atrophy via targeting of IGF-1 and PI3K(p85alpha), and that suppression of miR-29

189 Akt-mTOR and MAPK are downstream targets of IGF-1 signaling that are activated after brain injury.

190 ses in later life, understanding the role of IGFs during pregnancy in regulating placental resource a

191 The effect of platelet transfusions on IGF-1R was explored.

192 signaling with small-molecule inhibitors or IGF-1 withdrawal partially abrogates both the phosphoryl

193 These results demonstrate that overexpressed IGF-2 is the major tumorigenic driver in a subset of CRC

194 effects were specific to CRCs overexpressing IGF-2, as MEDI-573 did not affect the growth CRC cell li

195 d increased anabolic intracellular pathways (IGF-1-mTOR-p70S6sk-1 axis; MyoD) in muscles of trained a

196 2/IGF2, we find that IMP2 strongly promotes IGF action, by binding and stabilizing the mRNA encoding

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

198 Proximal IGF-1R signaling events, including IRS tyrosine phosphor

199 cy (LLE) in a series of 2-anilino-pyrimidine IGF-1R kinase inhibitors led to the identification of no

200 to the insulinlike growth factor 1 receptor (IGF-1R antibody) in patients with Ewing sarcoma family o

201 f the insulin-like growth factor 1 receptor (IGF-1R) and alterations in DNA repair rate, apoptosis, a

202 h the insulin-like growth factor 1 receptor (IGF-1R) and its close family member, the insulin recepto

203 IGF-1/insulin-like growth factor-1 receptor (IGF-1R) autocrine/paracrine signaling in patients with r

204 t the insulin-like growth factor 1 receptor (IGF-1R) controls this response in the central nervous sy

205 or of insulin-like growth factor 1 receptor (IGF-1R) in a panel of 22 protein kinases and in cells.

206 f the insulin like growth factor-1 receptor (IGF-1R) on neuronal differentiation and polarization in

207 t the insulin-like growth factor 1 receptor (IGF-1R) translocates to the cell nucleus, where it binds

208 th acquired resistance to an IGF-1 receptor (IGF-1R) tyrosine kinase inhibitor exhibited reduced expr

209 r the insulin-like growth factor 1 receptor (IGF-1R), in a subset of CRC tumors.

210 insulin-like growth factor type 1 receptor (IGF-1R).

211 f the insulin-like growth factor I receptor (IGF-IR) is a new therapeutic strategy to attenuate the u

212 e increased fetal norepinephrine and reduced IGF-1 and insulin.

213 multiple system atrophy patients and reduced IGF-1 brain levels in a transgenic mouse model of multip

214 ine kinases could not compensate for reduced IGF-1R activity in mitochondrial protection, and MCF-7 c

215 by 80% in these mice, which leads to reduced IGF signaling.

216 Serum and renal IGF-1 and EPO were significantly increased in UPI/OIR co

217 They also show that calorie restriction, IGF-1R signaling, and body temperature, three of the mai

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

219 ventional mice, in contrast, decreases serum IGF-1 and inhibits bone formation.

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

221 mechanism by which microbiota increase serum IGF-1.

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

223 lin/insulin-like growth factor-1 signalling (IGF-1) and insulin resistance (i.e. decreased insulin/IG

224 oth injury in mice with odontoblast-specific IGF-1 receptor ablation exhibited a reduced tertiary den

225 Subsequently, IGF-1-induced beta-catenin and PKM2 complex translocated

226 protection, and MCF-7 cells with suppressed IGF-1R activity became highly dependent on glycolysis fo

227 These new synthetic IGF-1 analogs are unique examples of disulfide bonds' ri

228 We show that systemic IGF-II treatments reverse the typical defects in social

229 Targeted IGF-1R knockout selectively in forebrain neurons reveale

230 eurons electroporated with a shRNA targeting IGF-1 receptor failed to migrate to the upper cortical l

231 ells electroporated with the shRNA targeting IGF-1 receptor were unable to form an axon and, therefor

232 cted by electroporation with shRNA targeting IGF-1 receptor.

233 ipts that are involved in WNT, HGF, TGFbeta, IGF, BMP, FGF and estrogen signaling.

234 We conclude that IGF-1 signaling is essential for sustaining cancer cell

235 nal precursor cells (HNPCs) demonstrate that IGF-1 stimulates a RIT1-dependent increase in Sox2 level

236 We also found that IGF-1 - mediated increase in epileptic activity led to n

237 We found that IGF-1R interacts with and phosphorylates PCNA in human e

238 ed to epilepsy, raising the possibility that IGF-1 may be epileptogenic.

239 Here we report that IGF-1 level in blood and IGF-1 signaling demonstrates ci

240 lectively in forebrain neurons revealed that IGF signaling also modulates calorie restriction-depende

241 Here we show that IGF-1 stimulates mitochondrial biogenesis in a range of

242 In neurons in culture we showed that IGF-1 receptor activation is important for growth cone a

243 These data suggest that IGF-1 promotes DNA repair in irradiated parotid glands t

244 We suggest that IGF-II represents a potential novel therapeutic target f

245 e, revealing tight co-expression between the IGF-IRa paralogues, but expression divergence comparing

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

247 inhibition of SirT-1 activity decreased the IGF-1-mediated resolution of DSB.

248 nt of its analogs as molecular tools for the IGF-1 receptor (IGF1-R) studies and as new therapeutics.

249 ts for most GPCRs, as yet unexplored for the IGF-1R, we sought to investigate specifically the regula

250 PK activation is selectively involved in the IGF-1 signaling, because another Ras protein, H-ras loca

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

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

253 Cells lacking the IGF-1 receptor remain arrested as multipolar forming a h

254 ice exhibited an increased expression of the IGF system and surfactant genes, which were decreased in

255 the intracellular pathways downstream of the IGF-1 receptor that contribute to these diverse physiolo

256 n2 isoform on expression and function of the IGF-1R.

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 These data suggest that citrate acts on the IGF-1R-AKT-PTEN-eIF2a pathway.

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

262 We conclude that the IGF-1/ephrinB1 axis plays significant roles in the early

263 utero electroporation, we show here that the IGF-1R is essential for neocortical development.

264 ro MS analysis of PCNA co-incubated with the IGF-1R kinase indicated tyrosine residues 60, 133, and 2

265 In particular, it assesses the impact of the IGFs and their signalling machinery on placental morphog

266 It also considers the role of the IGFs as environmental signals in linking resource availa

267 In agreement with this, IGF-1 robustly induced BNIP3 accumulation in mitochondri

268 4 and FUT8 expression, respectively, through IGF-1R/PI3K/Akt signaling pathway in human endometrial c

269 secretion via the regulated pathway and thus IGF-1R activation.

270 Thus, IGF-II may represent a novel potential therapy for ASD.S

271 rst demonstration to our knowledge of tissue IGF-1 regulation through proteolytic degradation and sug

272 ecrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.001).

273 Binding of beta-arrestin1 to IGF-1R leads to ligand-dependent degradation of the rece

274 the dynamic ribosomal biogenesis response to IGF-1, myotube diameter and protein accretion were susta

275 ty to increase glucose uptake in response to IGF-1.

276 on, and leads to a lack of responsiveness to IGF-1, cell cycle arrest and decreased viability of canc

277 P < 0.001) and a decrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.00

278 reted to reflect a heightened sensitivity to IGF-1 stimulation upon HFD feeding.

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

280 inflammation in conjunction with transgenic IGF-1 overexpression to improve postnatal growth.

281 In established tumors, IGF signaling is active, and NG2 inhibition targets cell

282 ich entails the solid-phase synthesis of two IGF-1 precursor chains that is followed by the Cu(I)-cat

283 The connection of the two IGF-1 precursor chains by the triazole-containing moieti

284 by promoting degradation of an unstimulated IGF-1R, but protecting the receptor against agonist-indu

285 These experiments revealed that vascular IGF-1R was down-regulated by platelet miR-223.

286 and serum and mRNA of liver and kidney VEGF, IGF-1, and erythropoietin (EPO) were determined.

287 In BTBR mice, IGF-II, via IGF-II receptor, but not via IGF-I receptor, reverses th

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

289 The effects of IGF-II occur via IGF-II receptors, and not IGF-I receptors, and target bo

290 0.001) and total RNA content (-16 +/- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.

291 uced 45S pre-rRNA expression (-64 +/- 5% vs. IGF-1; P < 0.001) and total RNA content (-16 +/- 2% vs.

292 lial injury through effects on vascular wall IGF-1R.

293 omarker of therapeutic dosing of AE, whereas IGF-1 is a key molecule coupled to gene expression of ot

294 ability, providing a novel mechanism whereby IGF-1 exerts antiatherogenic effects.

295 To determine mechanisms whereby IGF-1 reduces atherosclerosis and to explore the potenti

296 This prompted us to investigate whether IGF signaling is essential for mitochondrial maintenance

297 ough both isoforms co-immunoprecipitate with IGF-1R, the ligand-occupied receptor has greater affinit

298 s was increased after both AE and NMES, with IGF-1 being a signaling molecule that correlated with MC

299 Pretreatment with IGF-1 increased SirT-1 protein levels and increased deac

300 Primary skeletal myotubes were treated with IGF-1 (50 ng/ml) with or without 0.5 microM CX-5461 (CX)