ライフサイエンスコーパス: IGF-1

1 IGF-1 alone decreased Smad3 nuclearization and increased

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

3 IGF-1 did not alter engulfment by macrophages.

4 IGF-1 is thus a valid aid to antifibrotic treatment, wit

5 IGF-1 provoked phosphorylation and inactivation of PRAS4

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

7 IGF-1, IGFBP-3, and the molar ratio appeared to be posit

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

9 of insulin and insulin-like growth factor 1 (IGF-1) action in adipose tissue, we created mice lacking

10 urbance of the insulin-like growth factor 1 (IGF-1) axis.

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

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

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

14 as insulin and insulin-like growth factor 1 (IGF-1) likely modulate glycogen stores in astrocytes, bu

15 suggested that insulin-like growth factor 1 (IGF-1) or insulin-like growth factor binding protein 3 (

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

17 of the insulin/insulin-like growth factor 1 (IGF-1) signaling pathway.

18 rease in serum insulin-like growth factor 1 (IGF-1) that allows GH release from the pituitary.

19 tors RANKL and insulin-like growth factor 1 (IGF-1) to induce osteoclastogenesis in precursors.

20 the impact of insulin-like growth factor 1 (IGF-1) treatment on CDKL5 null mice to restore the synap

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

22 -regulation of insulin-like growth factor 1 (IGF-1), a hallmark of premature ageing.

23 erum levels of insulin-like growth factor 1 (IGF-1), a hormone with known actions on skeletal growth,

24 via binding of insulin-like growth factor 1 (IGF-1), an insulin-like hormone that is involved in gluc

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

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

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

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

29 hages released insulin-like growth factor 1 (IGF-1).

30 eptors for the insulin-like growth factor 1 (IGF-1).

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

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

33 Insulin-like growth factor-1 (IGF-1) and signal transducer and activator of transcript

34 ophage-derived insulin-like growth factor-1 (IGF-1) and tumor cell IGF-1 receptor (IGF-1R).

35 ic infusion of insulin-like growth factor-1 (IGF-1) exerts anti-inflammatory and antioxidant effects

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

37 Exogenous Insulin-Like Growth Factor-1 (IGF-1) is neuroprotective in animal models of brain inju

38 ed interest in insulin-like growth factor-1 (IGF-1) pathway activation as a potential therapeutic app

39 GH release and insulin-like growth factor-1 (IGF-1) production and/or release relative to pubertal gr

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

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

42 tion involving insulin-like growth factor-1 (IGF-1) signaling is simultaneously abolished.

43 a link to the insulin-like growth factor-1 (IGF-1) signaling pathway.

44 ncentration of insulin-like growth factor-1 (IGF-1) that primes the IGF-1 receptor (IGF-1R) but fails

45 evels of serum insulin-like growth factor-1 (IGF-1), leptin, and adiponectin using a random-effects m

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

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

48 98; IGFBP-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 a

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

50 mRNA expression of CD36 (-50%), CD14 (-43%), IGF-1 (-53%), and IL-6 (-40%) was reduced in CX3CR1-defi

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

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

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

54 We observed that the analysed IGF-1 mRNA splice variants were characterized by multimo

55 stosterone (-5.8%; 95% CI: -9.4, -2.0%), and IGF-1 (-5.9%; 95% CI: -8.3, -3.3%); and PFNA with IGF-1

56 stosterone (-6.6%; 95% CI: -10.1, -2.8%) and IGF-1 (-5.6%; -8.2, -2.9%); and PFNA and IGF-1 (-3.8%; 9

57 Here we report that VEGF-A and IGF-1 differ in their ability to stabilize newly formed

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

59 iated life span extension through BMAL1- and IGF-1-dependent mechanisms.

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

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

62 icant associations between endometriosis and IGF-1 (incidence rate ratio (IRR) = 0.88, 95% confidence

63 to the intricate relationship between GH and IGF-1, the relative contribution of each hormone to the

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

65 006 and analyzed for PFAS, sex hormones, and IGF-1.

66 Insulin and IGF-1 boost the process of glycogen formation.

67 Stimulation of cells with insulin and IGF-1 decreased cytosolic glucose concentration, likely

68 Insulin and IGF-1 enhance muscle protein synthesis through their rec

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

70 generated mice lacking both the insulin and IGF-1 receptor in myeloid cells (IR/IGF-1R(MKO)).

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

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

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

74 and IGF-1 (-5.6%; -8.2, -2.9%); and PFNA and IGF-1 (-3.8%; 95% CI: -6.4, -1.2%).

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

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

77 y across quartiles for both testosterone and IGF-1 in relation to PFOS, and for IGF-1 and PFNA in gir

78 PFAS and estradiol, total testosterone, and IGF-1 in 2,292 children (6-9 years of age) from the C8 H

79 20 and IGF-1 transcript levels in tumors and IGF-1 expression in tumor-associated B cells.

80 These studies reveal that VEGF and IGF-1 can have distinct inputs in the angiogenic process

81 ivation of pro-proliferative signals such as IGF-1, FGF-10, and BMP4.

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

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

84 Furthermore, knockdown of FoxM1 blocked IGF-1-mediated invasion, and dual targeting of IGF-1R an

85 unique inhibitor, NT157, which targets both IGF-1 receptor (IGF-1R) and STAT3, we show that these pa

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

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

88 and appearance of fibroblasts is favored by IGF-1 alone and in combination with the antifibrotic sub

89 ed PTPalpha phosphorylation, that induced by IGF-1 can occur in cells lacking Src family kinases (SFK

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

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

92 to the skeleton, which is likely mediated by IGF-1.

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

94 XCL2, STAT3, NUPR1, Jun, CSF1, CYR61, CEBPB, IGF-1, EGFR1, SPP1, and TGM2) within these important pat

95 -like growth factor-1 (IGF-1) and tumor cell IGF-1 receptor (IGF-1R).

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

97 r (GHR) results in reductions in circulating IGF-1 and hepatic steatosis, associated with systemic in

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

99 Endogenous cortical IGF-1 levels were unaffected by CDKL5 deletion.

100 It appears that ICR decreases IGF-1 and leptin and increases adiponectin in geneticall

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

102 ast cell protease 4 (MMCP-4), which degrades IGF-1.

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

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

105 s aspect should be considered when designing IGF-1-based treatments for neurodegenerative diseases.

106 e relative amount of mRNA encoding different IGF-1 alternative splicing variants.

107 he observed concentrations for the different IGF-1 mRNA splice variants in the cohort of tissues by e

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

109 sk among women aged <40 years at blood draw (IGF-1: IRR = 1.60, 95% CI: 0.86, 2.98; IGFBP-3: IRR = 1.

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

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

112 ed ERK1/2 phosphorylation in response to EGF/IGF-1 stimulation, resulting in induction of the cell cy

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

114 or, PTPalpha, and Abl in a complex to enable IGF-1-stimulated and Abl-dependent PTPalpha-Tyr-789 phos

115 activate PI3K in the presence of endogenous IGF-1.

116 We also evaluated a 5' distal weak enhancer (IGF-1 5'-upstream region growth hormone response element

117 H and increasing concentrations of exogenous IGF-1 triggers synergistic IRS1 tyrosine phosphorylation

118 The growth factor IGF-1 also stimulates PTPalpha-Tyr-789 phosphorylation t

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

120 king molecules, including the pivotal factor IGF-1, induced by TNF-alpha, IL-1beta and nitric oxide p

121 s, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma.

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

123 (95% CI: 0.57, 1.03; P for trend = 0.03) for IGF-1:IGFBP-3 ratio.

124 al (CI): 0.68, 1.23; P for trend = 0.31) for IGF-1, 1.33 (95% CI: 1.00, 1.76; P for trend = 0.04) for

125 ence--in models that included adjustment for IGF-1 concentrations (P for trend < 0.05).

126 erone and IGF-1 in relation to PFOS, and for IGF-1 and PFNA in girls.

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

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

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

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

131 in response to enhanced activation of the GH-IGF-1 axis.

132 mia promotes growth while suppressing the GH-IGF-1 axis.

133 wth Hormone/Insulin-like Growth Factor-1 (GH/IGF-1) pathway as well as pathways related to synapse fo

134 how bone cells integrate signals from the GH/IGF-1 to enhance skeletal mineralization and strength du

135 dehydroxamic acid (SAHA) or halofuginone +/- IGF-1.

136 e normal developmental maturation of hepatic IGF-1 intron 2 growth hormone response element (IN2GHRE)

137 etics around distal GHREs on the rat hepatic IGF-1 gene.

138 tored liver IGF-1 expression via the hepatic IGF-1 transgene.

139 with a recombinant adenovirus encoding human IGF-1.

140 Dilp8 is related to human IGF-1, and has been shown to coordinate tissue growth wi

141 Overall, these data suggest that, if IGF-1 or IGFBP-3 plays a role in the etiology of endomet

142 relevant, given the central role of the IGF1/IGF-1 receptor (IGF-1R) pathway in ES tumorigenesis and

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

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

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

146 ion, indicating the importance of Dexras1 in IGF-1 signaling in adipogenesis.

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

148 Expression of several factors, including IGF-1, FGF2, IL-1beta, and PDGF-A, was altered in TLR4-d

149 Indeed, IGF-1 lost its ability to stabilize neovessels when the

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

151 Folate uptake stimulated by insulin + IGF-1 was mediated by mTORC2 but did not involve mTORC1.

152 Insulin/IGF-1 signaling (IIS) pathway is known to control growth

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

154 nt status, by systemically affecting insulin/IGF-1 signalling, largely dictates stem cell proliferati

155 back signal that locally antagonizes insulin/IGF-1 signalling outputs in the germ line, regardless of

156 Alterations in cell-autonomous insulin/IGF-1 signaling in myeloid cells have recently been impl

157 dent on inhibition of DAF-16/FOXO by insulin/IGF-1 signalling (IIS).

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

159 worm with mutations in daf-2(e1370) insulin/IGF-1 signalling scales with lifespan.

160 Mechanistically, PDZ-RhoGEF enhanced insulin/IGF-1 signaling in adipose tissue by controlling ROCK-de

161 nd within tissues to otherwise equal insulin/IGF-1 signalling inputs, according to the needs for prod

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

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

164 through localized neutralization of insulin/IGF-1 signalling, requiring DAF-18/PTEN, but not DAF-16/

165 ants and treatments, such as reduced insulin/IGF-1 signaling and dietary restriction, which are criti

166 Reduced insulin/IGF-1 signalling (rIIS) extends lifespan across the evol

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

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

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

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

171 ated mice lacking the insulin receptor (IR), IGF-1 receptor (IGF1R), or both using Cre-recombinase dr

172 c ablation of GHR in which we restored liver IGF-1 expression via the hepatic IGF-1 transgene.

173 els of growth hormone (GH) and its mediator, IGF-1, associate with hepatic lipid accumulation.

174 centrations of the mRNAs for one or multiple IGF-1 alternative splicing isoforms.

175 Exogenous administration of IGF-1 rescued defective rpS6 phosphorylation, spine dens

176 The binding of IGF-1 to its receptor on non-professional phagocytes red

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

178 nded to reduce circulating concentrations of IGF-1 by 4% (149 +/- 2.6 compared with 144 +/- 2.5 ng/mL

179 plication of physiological concentrations of IGF-1 can increase rod photoreceptor sensitivity in mamm

180 sistent with these observations, deletion of IGF-1 receptor in airway epithelial cells led to exacerb

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

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

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

184 The dualistic nature of effects of IGF-1 treatment demonstrates that anabolic enhancement t

185 Pro-epileptic effects of IGF-1 were mediated by Akt-mTOR signaling.

186 Recent evidence of IGF-1 axis alteration in spinal muscular atrophy (SMA),

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

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

189 levels might raise T2DM risk independent of IGF-1 levels.

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

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

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

193 luated associations between plasma levels of IGF-1 and IGFBP-3 and laparoscopically confirmed endomet

194 CR-mediated changes in the plasma levels of IGF-1 and insulin.

195 hat PFAS are associated with lower levels of IGF-1 and sex hormones in young children.

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

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

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

199 y and associated epigenomic modifications of IGF-1 in a rodent model of multigenerational MetS.

200 ewly emerging concept that the modulation of IGF-1 receptor expression is a key event selectively det

201 In the presence of IGF-1, Erk activity persisted longer than in the presenc

202 ociated with T2DM incidence-and the ratio of IGF-1 to IGFBP-3 was inversely related with T2DM inciden

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

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

205 Restoration of IGF-1 improved overall insulin sensitivity and lipid pro

206 Here, we considered the role of IGF-1 in development of epilepsy after brain injury, usi

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

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

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

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

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

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

213 cates to the plasma membrane upon insulin or IGF-1 treatment, for which the unique C-terminal domain

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

215 Administration of OPN plus IGF-1 promotes regeneration as effectively as downregula

216 Postnatal IGF-1 expression is transcriptionally regulated by growt

217 ate set of engineered ligaments, recombinant IGF-1, but not GH, enhanced collagen content and mechani

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

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

220 sting that SFK activity dominantly regulates IGF-1/IGF-1 receptor signaling to PTPalpha.

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

222 ed to support an enduring vascular response, IGF-1 stabilized neovessels generated from primary endot

223 , products of microbial metabolism, restores IGF-1 and bone mass to levels seen in nonantibiotic-trea

224 Serum IGF-1 levels were genotype- and sex-dependent.

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

226 ne growth restriction (IUGR) decreases serum IGF-1 levels.

227 mechanism by which microbiota increase serum IGF-1.

228 gy sensing pathways, including reduced serum IGF-1, increased AMPK activity, and decreased AKT, TOR,

229 In cells expressing SFKs, IGF-1-stimulated phosphorylation of PTPalpha is mediated

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

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

232 autonomous fashion to regulate GH-stimulated IGF-1 expression in the liver of neonatal mice, which pl

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

234 , but not early, infarct size by suppressing IGF-1 degradation and, consequently, diminished cardiac

235 Src and Fyn in SFK-deficient cells switches IGF-1-induced PTPalpha phosphorylation to occur in an Ab

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

237 n increase in the miR-133a potential target, IGF-1 receptor, along with hyperactivation of Akt signal

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

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

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

241 thin a few days of injury but that long-term IGF-1 treatment was pro-epileptic.

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

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

244 Here we demonstrate that IGF-1/IGF-IR regulates PKM2 expression by enhancing HIF-

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

246 We found that IGF-1 was neuroprotective within a few days of injury bu

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

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

249 e genetic and functional studies reveal that IGF-1- and microvesicle-dependent communication between

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

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

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

253 Moreover, our data suggest that IGF-1 treatment could be a promising candidate for clini

254 95% CI: 0.80, 1.57; Ptrend = 0.51), and the IGF-1:IGFBP-3 molar ratio (IRR = 0.94, 95% CI: 0.66, 1.3

255 protein RACK1 and that RACK1 coordinates the IGF-1 receptor, PTPalpha, and Abl in a complex to enable

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

257 herefore, reducing rather than enhancing the IGF-1 pathway could constitute a useful strategy to limi

258 esis that reducing rather than enhancing the IGF-1 signaling pathway exerts a neuroprotective effect

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

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

261 rformance of our method by interrogating the IGF-1/AKT signaling pathway, showing that even rarely ob

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

263 of the insulin receptor (M-IR-/- mice), the IGF-1 receptor (M-IGF1R-/- mice), or both (MIGIRKO mice)

264 Moreover, increased methylation of the IGF-1 P2 transcriptional start site among IUGR lineage F

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

266 t that Dexras1 is a critical mediator of the IGF-1 signal to activate MAPK, linking glucocorticoid si

267 like growth factor-1 (IGF-1) that primes the IGF-1 receptor (IGF-1R) but fails to promote tyrosine ph

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

269 We show that this IGF-1-stimulated tyrosine kinase is Abl.

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

271 monstrates that anabolic enhancement through IGF-1 activation of mTOR cascade can be beneficial or ha

272 hways, and increasing muscle growth, through IGF-1/2 and TGF-beta signaling pathways, are potential s

273 ficant increases in liver and adipose tissue IGF-1 production.

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

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

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

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

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

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

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

281 te MAPK, linking glucocorticoid signaling to IGF-1 signaling in adipogenesis.

282 do not confirm an association between total IGF-1 concentrations and risk of T2DM in the general stu

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

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

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

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

287 In contrast to VEGF, IGF-1 stabilizes neovessels, which is dependent on Erk a

288 0.001) and total RNA content (-16 +/- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.

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

290 ater than resting serum (P < 0.001), whereas IGF-1 was not elevated at this time point (P = 0.21 vs.

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

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

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

294 mad3 to the nucleus, also when combined with IGF-1.

295 Guided fibrosis with IGF-1 and antifibrotic substances might maintain corneal

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

297 (-5.9%; 95% CI: -8.3, -3.3%); and PFNA with IGF-1 (-3.5%; 95% CI: -6.0, -1.0%).

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

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

300 ackground, the keratocytes were treated with IGF-1, and suberoylanilidehydroxamic acid (SAHA) or halo