ライフサイエンスコーパス: IGF-1 receptor

1 hat IGF-2 did not signal exclusively via the IGF-1 receptor.

2 0 and Hsp60 suppressed polyubiquitination of IGF-1 receptor.

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

4 ntly reduced tyrosine phosphorylation by the IGF-1 receptor.

5 f Twist in the anti-apoptotic actions of the IGF-1 receptor.

6 nvolved in the anti-apoptotic actions of the IGF-1 receptor.

7 layer of the epidermis and activation of the IGF-1 receptor.

8 action, consistent with its affinity for the IGF-1 receptor.

9 prevention of interaction with cell membrane IGF-1 receptors.

10 docking protein for both the insulin and the IGF-1 receptors.

11 istent with the nonpolarized distribution of IGF-1 receptors.

12 ects on its interaction with the insulin and IGF-1 receptors.

13 horylation of IRS-1 and IRS-2 by insulin and IGF-1 receptors.

14 age in heterodimer formation with insulin or IGF-1 receptors.

15 substrate mediating the mitogenic actions of IGF-1 receptors.

16 endocytosis via either wild-type or chimeric IGF-1 receptors.

17 ed, by virtue of the compensatory actions of IGF-1 receptors.

18 jor cytoplasmic substrate of the insulin and IGF-1 receptors.

19 d GSK3beta, and this is dependent on insulin/IGF-1 receptors.

20 ated granule cells through the activation of IGF-1 receptors.

21 nd with and without knock-out of insulin and IGF-1 receptors.

22 r, but not the insulin-like growth factor 1 (IGF-1) receptor.

23 ptor, i.e. the insulin-like growth factor I (IGF-1) receptor.

24 ylation by the insulin-like growth factor-1 (IGF-1) receptor.

25 status of the insulin-like growth factor 1 (IGF-1) receptor.

26 he insulin and insulin-like growth factor-1 (IGF-1) receptors.

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

28 cruited to the insulin-like growth factor 1 (IGF-1) receptor, a receptor tyrosine kinase, upon agonis

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

30 In contrast, stimulating the IGF-1 receptors accelerates granule cell migration durin

31 Insulin and IGF-1 receptors activate Akt to a similar extent, wherea

32 Furthermore, DETC-deficient mice had reduced IGF-1 receptor activation at wound sites.

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

34 ion in IGF-1R expression, demonstrating that IGF-1 receptor activation was involved in this process.

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

36 bunit, characteristic of polarized RPE, with IGF-1 receptor alpha and beta subunits exhibiting a nonp

37 Xp-HB-IGF-1 activated the IGF-1 receptor and Akt with identical kinetics and dose

38 s with IGF-1 and inhibits its binding to the IGF-1 receptor and hence negatively regulates the PI3K-A

39 ase in cells expressing the chimeric insulin/IGF-1 receptor and in cells derived from the insulin rec

40 F-1 receptors in fat (FIGIR-KO, fat-specific IGF-1 receptor and insulin receptor-KO) exhibit complete

41 The increased adiposity and elevated IGF-1, IGF-1 receptor and PPARgamma mRNAs were not seen in the

42 ransgene expression led to activation of the IGF-1 receptor and spontaneous tumorigenesis in prostate

43 and either the alpha or beta subunits of the IGF-1 receptor and visualized in Z-section using confoca

44 ted with a decreased presence of insulin and IGF-1 receptors and accumulation of nitrotyrosin in neur

45 e, IGF-1 treatment caused phosphorylation of IGF-1 receptors and increased the levels of the phosphat

46 Insulin receptors, as well as IGF-1 receptors and their postreceptor signaling partner

47 protein of the insulin-like growth factor-1 (IGF-1) receptor and of the insulin receptor.

48 ress c-Met and insulin-like growth factor-1 (IGF-1) receptors and synthesize and secrete the correspo

49 These pups also had elevated muscle IGF-1, IGF-1 receptor, and PPARgamma mRNA levels, which may ind

50 urbation of the balance between IGF-1/2, the IGF-1 receptor, and the IGF-binding proteins (IGFBPs) le

51 levels in beta cells than either insulin or IGF-1 receptors, and it has been shown to engage in hete

52 utricular epithelial cells expressed FGF and IGF-1 receptors, and utricular hair cells produced FGF-2

53 Moreover, infusion of a selective IGF-1 receptor antagonist abrogates HIF-1alpha accumulat

54 sed by intracerebroventricular injections of IGF-1 receptor antagonist JB-1.

55 Here we show that an IGF-1 receptor antagonist suppresses retinal neovascular

56 in-like growth factor (IGF)-1 and the type I IGF-1 receptor are important regulators of vascular func

57 nfer that interactions between IGF-1 and the IGF-1 receptor are necessary for induction of maximal ne

58 (1) insulin-like growth factor-1 (IGF-1) and IGF-1 receptor are targets of miR-1; (2) miR-1 and IGF-1

59 nd enhanced signaling through hybrid insulin/IGF-1 receptor as important mechanisms underlying aldost

60 n synthesis, and it inhibited ligand-induced IGF-1 receptor autophosphorylation.

61 replacement of the C-terminal domain of the IGF-1 receptor beta-subunit with the corresponding segme

62 ging gene Klotho and less phosphorylation of IGF-1 receptor beta.

63 g kidneys, IGF-1 mRNA and peptide levels and IGF-1 receptor binding were unaltered.

64 the absence of IGF-1, growth hormone, and an IGF-1 receptor-blocking antibody.

65 Estradiol-induced rescue of LTP requires the IGF-1 receptor, but not the classical estrogen receptors

66 Stimulation of insulin and IGF-1 receptors by insulin caused a temporary dissociati

67 The abundance of cardiac IGF-1 receptor can be upregulated by Hsp60, but how diab

68 e to lack of insulin receptors suggests that IGF-1 receptors cannot effectively mediate all the metab

69 ntrol beta-cells exhibited low expression of IGF-1 receptors compared to compensatory upregulation in

70 we show that expression of normal insulin or IGF-1 receptors confers cells with abilities to reduce e

71 ggest that dysfunctions of brain insulin and IGF-1 receptors contribute to Abeta aggregation and subs

72 In C. elegans, the sole insulin/IGF-1 receptor, DAF-2, negatively regulates the FOXO tra

73 strains with reduced function in the insulin/IGF-1 receptor, DAF-2, various insulins (INS-1 and INS-1

74 , in vivo studies reveal that inhibiting the IGF-1 receptors decelerates granule cell migration durin

75 are strikingly similar to the phenotypes of IGF-1 receptor-deficient mice and suggest that Akt may s

76 engineered for conditional disruption of the IGF-1 receptor (DeltaIGF-1R).

77 These Wnt effects are insulin/IGF-1 receptor-dependent and are lost in insulin/IGF-1 r

78 ver, neutralizing antibody to TGF-beta or to IGF-1 receptor did not suppress increases in laminin C1

79 1 receptor-dependent and are lost in insulin/IGF-1 receptor double knock-out cells.

80 the most critical downstream effector of the IGF-1 receptor during development.

81 rylated, we examined whether pp120 regulates IGF-1 receptor endocytosis in transfected NIH 3T3 cells.

82 pp120 failed to alter IGF-1 receptor endocytosis via either wild-type or chime

83 s one of the mechanisms by which insulin and IGF-1 receptors exert different effects on gene expressi

84 To investigate how the insulin and IGF-1 receptors exert specificity in their biological re

85 Knockdown of IGF-1 receptor expression by RNA interference reduced th

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

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

88 IGF-1 receptor failed to phosphorylate pp120 in response

89 1 in alveolar fibroblasts or deletion of the IGF-1 receptor from ILC precursors interrupted ILC3 biog

90 H-terminal fragment (CTF), insulin receptor, IGF-1 receptor, glycogen synthase kinase 3-beta (GSK-3be

91 with combined deficiency of both insulin and IGF-1 receptors have a coordinated down-regulation of ge

92 d by the insulin/insulin-like growth factor (IGF)-1 receptor homolog DAF-2, which signals through a c

93 y relatively strong mutations in the insulin/IGF-1 receptor homolog daf-2.

94 , which acts downstream of the DAF-2 insulin/IGF-1 receptor homolog.

95 g via the FOXO homolog DAF-16 or the insulin/IGF-1-receptor homolog DAF-2.

96 Mutants with reduced activity of the insulin/IGF-1-receptor homologue DAF-2 have been shown to live t

97 Signaling by the insulin-like growth factor (IGF)-1 receptor (IGF-1R) has been implicated in the prom

98 In mice, haploinsufficiency of the IGF-1 receptor (IGF-1R(+/-)), at a whole-body level, inc

99 that both pharmacological inhibition of the IGF-1 receptor (IGF-1R) and deprivation of IGF-1 potenti

100 echanisms involved in the cross-talk between IGF-1 receptor (IGF-1R) and estrogen receptor signaling

101 In addition, the signaling links between IGF-1 receptor (IGF-1R) and estrogen receptors (ERs), wh

102 tment resulted in phosphorylation of uterine IGF-1 receptor (IGF-1R) and formation of an IGF-1R/insul

103 bers of the insulin-like growth factor (IGF)/IGF-1 receptor (IGF-1R) and IL-6 receptor (IL-6R) signal

104 lation, identified neurons that express both IGF-1 receptor (IGF-1R) and insulin receptor transcripts

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

106 examined the role of cross talk between the IGF-1 receptor (IGF-1R) and the epidermal growth factor

107 determine whether E2 also interacts with the IGF-1 receptor (IGF-1R) and to determine the cellular lo

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

109 lin-like growth factor-1 (IGF-1), IGF-2, and IGF-1 receptor (IGF-1R) by investigating their expressio

110 owed <25% (125)I-IGF-1 surface binding, <20% IGF-1 receptor (IGF-1R) expression than that of normal m

111 Expression of IGF-1 and IGF-1 receptor (IGF-1R) genes was identified from H9A RN

112 Akt activation by the IGF-1 receptor (IGF-1R) has been posited to be a mechani

113 s provide further evidence for a role of the IGF-1 receptor (IGF-1R) in suppressing UVB-induced carci

114 Gene expression of IGF-1 and IGF-1 receptor (IGF-1R) in the ischemic brain tissue wer

115 vate insulin receptors (IR-A and -B) and the IGF-1 receptor (IGF-1R) is crucial for understanding the

116 increases (p<0.05) in the expression of both IGF-1 receptor (IGF-1R) mRNA and protein.

117 We recently demonstrated that reducing IGF-1 receptor (IGF-1R) numbers in the endothelium enhan

118 f IGF-1 are predominantly transduced through IGF-1 receptor (IGF-1R) on the cilia of fibroblasts and

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

120 analysis of all the pathways mediated by the IGF-1 receptor (IGF-1R) remains lacking.

121 We hypothesized that IGF-1 receptor (IGF-1R) signaling disrupts the POU1F1/CB

122 +) T cells through insulin receptor (IR) and IGF-1 receptor (IGF-1R) signaling.

123 ted mice lacking either GH receptor (GHR) or IGF-1 receptor (IGF-1R) specifically in skeletal muscle.

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

125 tor 1 (IGF-1) on protein turnover and of the IGF-1 receptor (IGF-1R) were examined in skeletal muscle

126 analysis for IGF binding protein 3 (IGFBP3), IGF-1 receptor (IGF-1R), Akt, extracellular signal-relat

127 es, such as IGF binding protein-5 (IGFBP-5), IGF-1 receptor (IGF-1R), and phosphoinositide 3-kinase (

128 been ascribed to the IGF-1 and its receptor, IGF-1 receptor (IGF-1R), and subsequent activation of th

129 growth factors (IGF-1 and IGF-2) bind to the IGF-1 receptor (IGF-1R), increasing cell proliferation a

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

131 GF-1, leading to increased activation of the IGF-1 receptor (IGF-1R).

132 53 at critical targets such as Nanog and the IGF-1 receptor (IGF-1R).

133 is mediated via insulin receptors (InsRs) or IGF-1 receptors (IGF-1Rs) in the brain.

134 opoiesis but given the broad distribution of IGF-1 receptors (IGF-1Rs), its mechanism of action has r

135 g in the heart is transduced via insulin and IGF-1 receptors (IGF-1Rs).

136 in cells overexpressing a dominant negative IGF-1 receptor, IGF-1 failed to increase Twist expressio

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

138 Insulin-like growth factor (IGF) 1 receptor (IGF1R)-mediated signaling plays key rol

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

140 e used a Cre/loxP system in which the type 1 IGF-1 receptor (Igf1r) has been disrupted specifically i

141 Mice with knockout of the IGF-1 receptor (Igf1r) in their pre-osteoblastic cells s

142 IGF-1 through the insulin receptor (IR) and IGF-1 receptor (IGF1R) maintain muscle mass via suppress

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

144 IGF-1 receptor (IGF1R) signaling promotes keratinocyte p

145 ed from the IGF-1.IGFBP3 complex to activate IGF-1 receptor (IGF1R) signaling.

146 ke growth factors (IGFs) and their receptor, IGF-1 receptor (IGF1R), have important roles in growth,

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

148 lls expressing either insulin receptor (IR), IGF-1 receptor (IGF1R), or chimeric IR-IGF1R receptors.

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

150 inactivated both insulin receptors (IRs) and IGF-1 receptors (IGF1Rs) in the hippocampus (Hippo-DKO)

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

152 F-1, infusion of IGF-1:TTC reduced levels of IGF-1 receptor immunoreactivity in the same extracts.

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

154 To establish a role for the Igf-1 receptor in beta-cells, we intercrossed mice heter

155 and studied how diabetes modulates Hsp60 and IGF-1 receptor in diabetic myocardium.

156 Thus, while neither the insulin receptor nor IGF-1 receptor in muscle is critical for glucose homeost

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

158 Mice lacking insulin and IGF-1 receptors in fat (FIGIR-KO, fat-specific IGF-1 rec

159 indicate that (i) the potency of insulin and IGF-1 receptors in stimulating glycogen synthesis correl

160 that insulin receptors are more potent than IGF-1 receptors in stimulating glycogen synthesis.

161 ted sprouting, and the presence of activated IGF-1 receptors in the vasculature was revealed by immun

162 n receptor and insulin-like growth factor 1 (IGF-1) receptor in cardiac and skeletal muscle develop e

163 to insulin and insulin-like growth factor-1 (IGF-1) receptors in PC12 cells and NIH-3T3 cells overexp

164 These data indicate that activation of the IGF-1 receptor increases lipogenesis in SEB-1 cells thro

165 ent of Akt activation mediated by insulin or IGF-1 receptors, indicating that the effect of insulin o

166 ch is blocked by insulin-like growth factor (IGF)-1 receptor inhibitor and mammalian target of rapamy

167 Finally, we show that the Igf-1 receptor inhibitor linsitinib reverses the pain be

168 can be selectively ablated by treatment with IGF-1 receptor inhibitors or chromatin-modifying agents,

169 in Leu-17 --> Pro) that allowed for a strong IGF-1-receptor interaction.

170 Insulin and IGF-1 receptors (IR and IGF1R) are highly homologous and

171 Like the insulin receptor, the IGF-1 receptor is a heterotetrameric receptor tyrosine k

172 ratinocytes grown in conditions in which the IGF-1 receptor is inactive inappropriately replicate in

173 esults indicate that IRS-1 (activated by the IGF-1 receptor) is one of several proteins that regulate

174 Expression of the dominant negative IGF-1 receptor (K1003R) also abolished DCA-induced AKT a

175 4 and by expression of the dominant negative IGF-1 receptor (K1003R), which inhibited in trans.

176 In addition, both CKD and IGF-1 receptor knockout mice developed fibrosis in regen

177 ell function in CKD, we created an inducible IGF-1 receptor knockout mouse and found impaired satelli

178 This phosphorylation of IGF-1 receptor led to increased phosphorylation of Akt a

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

180 components of the IGF pathway, namely IGF-1, IGF-1 receptor, mammalian/mechanistic target of rapamyci

181 he insulin and insulin-like growth factor-1 (IGF-1) receptors mediate signaling for energy uptake and

182 lin secretion from the beta cells through an IGF-1 receptor-mediated pathway.

183 IGF-1 activation of IGF-1 receptor, Mek, and Akt were reduced accordingly in

184 IGF-1 receptor mRNA and IGF-1 receptor number and affini

185 IGF-1 receptor mRNA levels and IGF-1 receptor number bot

186 The daf-2 Insulin/IGF-1 receptor mutant exhibits a significant extension o

187 )[PheB25 alpha-carboxamide]insulin for these IGF-1 receptor mutants is reduced only 4- and 50-fold, r

188 factor DAF-16, is required for daf-2-insulin/IGF-1 receptor mutations to extend life-span.

189 idylinositol 3-OH kinase) and daf-2 (insulin/IGF-1 receptor) mutations, on associative learning behav

190 This effect was inhibited by the IGF-1 receptor neutralizing antibody aIR3, the PI-3K inh

191 ells overexpressing insulin (NIH-3T3(IR)) or IGF-1 receptor (NIH-3T3(IGF-1R)).

192 IGF-1 receptor mRNA and IGF-1 receptor number and affinity were not different am

193 IGF-1 receptor mRNA levels and IGF-1 receptor number both fell.

194 NIH-3T3 fibroblasts overexpressing the human IGF-1 receptor (NWTb3), treatment with IGF-1 (10(-8) m)

195 ed diabetic rat, downregulation of Hsp60 and IGF-1 receptor occurred 4 days after induction of diabet

196 d an increase in tyrosine phosphorylation of IGF-1 receptor on 1135/1136.

197 effects of a small molecule inhibitor of the IGF-1 receptor on chronic UVB radiation.

198 inocytes do not express IGF-1, and hence the IGF-1 receptor on keratinocytes is activated by IGF-1 se

199 Basic research implicating the IGF-1 receptor on the CD-34+ orbital fibrocyte in the pa

200 ation in CHO cells overexpressing either the IGF-1 receptor or epidermal growth factor receptor.

201 By contrast, mice lacking the IGF-1 receptor or the IGF-1 receptor plus one Ir allele

202 sulin sensitivity may reflect the absence of IGF-1 receptors or increased triglyceride levels in the

203 tle binding, if any, of the peptide with the IGF-1 receptors or the epidermal growth factor receptors

204 were assayed for insulin-like growth factor (IGF)-1 receptor phosphorylation (IGF-1Rphos).

205 IGF-1 receptor phosphorylation and coimmunoprecipitation

206 expression and plasma levels and increasing IGF-1 receptor phosphorylation in muscle may explain the

207 ptor substrate-1 phosphorylation by 34%, but IGF-1 receptor phosphorylation was unaffected.

208 of insulin and insulin-like growth factor-1 (IGF-1) receptors play a role in aggregation of Abeta.

209 rast, mice lacking the IGF-1 receptor or the IGF-1 receptor plus one Ir allele appear normal.

210 Our results reveal that Igf-1 receptors promote beta-cell development and surviv

211 beta-Arrestins bind to the ligand-occupied IGF-1 receptors, promote their endocytosis, and enhance

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

213 Placental IGF-1 receptor protein was positively associated with se

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

215 In healthy cells, activation of insulin and IGF-1 receptor reduces the extracellular ADDLs applied t

216 IGF-1 receptor regulation of VEGF action is mediated at

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

218 Insulin and insulin-like growth factor 1 (IGF-1) receptors share many downstream signaling pathway

219 ivation of the insulin-like growth factor-1 (IGF)-1 receptor signaling pathways by IGF-1 and IGF-2 re

220 ity and maintain viability via engagement of IGF-1 receptor signaling and an altered chromatin state

221 d critical roles of highly conserved insulin/IGF-1 receptor signaling in determining health outcomes

222 We investigated the changes of Hsp60 and IGF-1 receptor signaling in the diabetic myocardium and

223 Insulin and IGF-1 receptor signaling is sufficient to determine esse

224 e data suggest that persistent activation of IGF-1 receptor signaling pathways in basal epithelial ce

225 e 3-kinase is a key component of insulin and IGF-1 receptor signaling pathways, activation of this li

226 Heat shock protein (Hsp)60 and IGF-1 receptor signaling protect cardiac muscle against

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

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

229 ulation of Hsp60 and subsequent reduction of IGF-1 receptor signaling.

230 Insulin and insulin-like growth factor 1 (IGF-1) receptor signaling pathways differentially modula

231 get of insulin/insulin-like growth factor 1 (IGF-1) receptor signaling, are responsible for metabolic

232 h proposed GIGYF1 enhancement of insulin and IGF-1 receptor signalling.

233 The IGF-1 effect was specific for the IGF-1 receptor since, in cells overexpressing a dominant

234 oles, we delete insulin receptor (SMIRKO) or IGF-1 receptor (SMIGF1RKO) in VSMC and in mice.

235 Mice that express a dominant-negative IGF-1 receptor, specifically in skeletal muscle (MKR mic

236 urs in response to PDGF receptor and insulin/IGF-1 receptor stimulation.

237 gnificantly increased phosphorylation by the IGF-1 receptor, suggesting that basal phosphorylation of

238 cal for insulin binding are conserved in the IGF-1 receptor, suggesting that they may play a role in

239 how that T(24) fails to be phosphorylated by IGF-1 receptors, suggesting that this residue is targete

240 and an insulin-like growth factor 1 (IGF-1)-IGF-1 receptor system that can be activated to induce th

241 ess the insulin-like growth factor-1 (IGF-1)-IGF-1 receptor system, and IGF-1 can be tethered to self

242 Although HUVEC have many more IGF-1 receptors than insulin receptors (approximately 40

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

244 ound to enhance mRNA levels of IGF-1 and the IGF-1 receptor, the latter of which appeared to be respo

245 or no insulin receptor but large amounts of IGF-1 receptor, these data strongly suggest a new regula

246 bly less potent than IGF-1 in activating the IGF-1 receptor, they were equipotent stimulators of ERK1

247 e cell migration by altering the activity of IGF-1 receptors through modification of cerebellar IGF-1

248 pport a model whereby estradiol acts via the IGF-1 receptor to maintain the functional integrity of h

249 a in ovariectomized female rats acts via the IGF-1 receptor to protect the functional integrity of CA

250 uble tissue-specific knockout of insulin and IGF-1 receptors to eliminate all insulin/IGF-1 signallin

251 igate the different abilities of insulin and IGF-1 receptors to stimulate glycogen synthesis.

252 way is insensitive to chemical inhibition of IGF-1 receptor tyrosine kinase activity.

253 eceptor signaling, beta-arrestins couple the IGF-1 receptor tyrosine kinase to the phosphatidylinosit

254 trate specific for the insulin vis-a-vis the IGF-1 receptor tyrosine kinase, the pp120 signaling path

255 ted whether pp120 is also a substrate of the IGF-1 receptor tyrosine kinase.

256 The insulin-like growth factor-1 (IGF-1)/receptor tyrosine kinase recently has been shown

257 nockout of the insulin receptor (VENIRKO) or IGF-1 receptor (VENIFARKO).

258 tance syndrome, or inhibition of insulin and IGF-1 receptors via pharmacological reagents increases A

259 on was decreased in type 1 diabetes, whereas IGF-1 receptor was decreased in both models, as were Akt

260 , a tyrosine kinase inhibitor of insulin and IGF-1 receptor, was shown to inhibit annexin II secretio

261 ed against the insulin-like growth factor 1 (IGF-1) receptor, was recently approved by the United Sta

262 s of insulin and insulin-like growth factor (IGF)-1 receptors, we asked whether these new proteins, t

263 insulin, as found in MDI, will activate the IGF-1 receptor, we sought to determine if IGF-1 is capab

264 iency on the changes of myocardial Hsp60 and IGF-1 receptor, we used phlorizin to normalize blood glu

265 Similar changes of Hsp60 and IGF-1 receptor were observed in the skeletal muscle of S

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

267 ing alanine-substituted secreted recombinant IGF-1 receptors were expressed in 293 EBNA cells, and th

268 ase and phosphorylation of insulin, EGF, and IGF-1 receptors were not altered.

269 n showed no significant interaction with the IGF-1 receptor, while a chimeric proinsulin containing t

270 C-terminal domain of the beta-subunit of the IGF-1 receptor with the corresponding fragment in the in