ライフサイエンスコーパス: IGF-I receptor

1 h muscle require autocrine activation of the IGF I receptor.

2 ne kinase activity of the IR, but not of the IGF-I receptor.

3 unocapture, PC-1 was not associated with the IGF-I receptor.

4 insulin-like growth factor I (IGF-I) and the IGF-I receptor.

5 is evident in fibroblasts overexpressing the IGF-I receptor.

6 owth of fibrosarcomas that overexpressed the IGF-I receptor.

7 sforming ability of cells overexpressing the IGF-I receptor.

8 otein expression patterns of IGFBP-5 and the IGF-I receptor.

9 d transcription of the VEGF gene and via the IGF-I receptor.

10 nduced phosphorylation and activation of the IGF-I receptor.

11 this effect of IGF-I is mediated through the IGF-I receptor.

12 kt and p70(s6k) independent of a functioning IGF-I receptor.

13 that IGF-I effects are mediated through the IGF-I receptor.

14 sfected with ER alpha, both of which express IGF-I receptor.

15 3 (NWTb3) cells, which overexpress the human IGF-I receptor.

16 3T3 cells overexpressing a dominant-negative IGF-I receptor.

17 These actions are mediated by the IGF-I receptor.

18 onstrated that H838 tumors express IGF-I and IGF-I receptors.

19 IGF-I and a sufficient number of functional IGF-I receptors.

20 RS-4 in mouse NIH-3T3 cells that overexpress IGF-I receptors.

21 ia formation of hybrids with the insulin and IGF-I receptors.

22 YF1 dissociates, but Grb10 remains linked to IGF-I receptors.

23 the insulin and insulin-like growth factor (IGF)-I receptors.

24 the insulin and insulin-like growth factor (IGF)-I receptors.

25 pressed slightly more insulin receptors than IGF-I receptors (120,000 versus 100,000).

26 igration of these two cell types through the IGF-I receptor; 2) interaction of vitronectin with the a

27 cytes expressed fewer insulin receptors than IGF-I receptors (20,000 versus 60,000), but during diffe

28 y of the IGF response was confirmed using an IGF-I receptor Ab, and additional studies demonstrated t

29 250 and 1251 in the carboxyl terminus of the IGF-I receptor abrogates IGF-I-induced cellular prolifer

30 Insulin-like growth factor-I (IGF-I) receptors activate divergent signaling pathways b

31 mal human intestinal smooth muscle cells the IGF-I receptor activates a heterotrimeric G protein and

32 he insulin and insulin-like growth factor I (IGF-I) receptor activates the phosphoinositide-3-kinase/

33 Insulin-like growth factor (IGF)-I receptor activation leads to enhanced proliferati

34 ntial points in the cell death cascade where IGF-I receptor activation may afford neuroprotection.

35 ar proliferation in cells overexpressing the IGF-I receptor alone but had an even greater proliferati

36 In cells, overexpressing IGF-I receptors alone, IGF-I addition enhanced cellular

37 inhibitory antibody for the alpha subunit of IGF-I receptor (alphaIR3).

38 Impaired signaling through the IGF-I receptor also did not decrease the ability of MyoD

39 has been shown to interact with insulin and IGF-I receptors, although the role of SH2-B in these sig

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

41 as early events in differentiation, and the IGF-I receptor and downstream signaling molecules, inclu

42 murine CSMN axon outgrowth, mediated via the IGF-I receptor and downstream signaling pathways; this i

43 inear relationship between activation of the IGF-I receptor and induction of VEGF mRNA.

44 B1 reduction decreased the expression of the IGF-I receptor and IRS-1 in MCF-7 but not in MDA MB-231

45 to fully activate the kinase activity of the IGF-I receptor and phosphorylate IRS-1.

46 Subsequently, SHP-2 is transferred to IGF-I receptor and regulates the duration of IGF-I recep

47 associated with a lack of SHP-2 transfer to IGF-I receptor and sustained receptor phosphorylation.

48 rough pathways apparently independent of the IGF-I receptor and that activation of the IGF-I receptor

49 results suggest that activation of both the IGF-I receptor and the alpha5beta1 integrin is required

50 C2BP5 that is dependent on activation of the IGF-I receptor and the phosphatidyl inositol 3-kinase (P

51 data suggest that receptor crosstalk between IGF-I receptors and ER alpha has an important role in ne

52 s at sites specific for IGF-I, and that both IGF-I receptors and IGF-I binding proteins are present i

53 In cells overexpressing IGF-I receptors and IRS-4, the effect of IGF-I in overco

54 tive effect in cells overexpressing both the IGF-I receptors and IRS-4.

55 the major substrates of both the insulin and IGF-I receptors and is generally localized in the cytoso

56 id rafts, anti-beta2M mAbs excluded IL-6 and IGF-I receptors and their substrates from the rafts.

57 ermine whether Grb10 links other proteins to IGF-I receptors and thus modulates IGF-I signaling.

58 ls of the type 1 insulin-like growth factor (IGF-I) receptor and do not express insulin receptor subs

59 Insulin-like growth factor-I (IGF-I) receptors and insulin receptors belong to the sam

60 97 kDa, representing the beta-subunit of the IGF-I receptor, and a predominant tyrosyl-phosphorylated

61 Expression of insulin receptor, IGF-I receptor, and SCF was studied in gastric muscles a

62 e phosphorylation of the beta subunit of the IGF-I receptor, and the magnitude of this response was c

63 kinase in phosphorylating and activating the IGF-I receptor, and this receptor phosphorylation and ac

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

65 ty, decline in insulin-like growth factor-I (IGF-I) receptor, and lower histone-4 mRNA expression.

66 rons expressed insulin-like growth factor-I (IGF-I) receptors, and deltaFADD-mediated survival of gra

67 e effects of the insulin-like growth factor (IGF)-I receptor antagonist AG1024 were investigated in c

68 In the present study, an IGF-I receptor antagonist (JB3) was synthesized, and its

69 E(2) or IGF-I in the presence of either the IGF-I receptor antagonist JB1 or the ER antagonist ICI 1

70 The ER and IGF-I receptor antagonists similarly blocked the E(2)-in

71 in cultured tubular cells, and neutralizing IGF-I-receptor antibodies partially inhibit this activit

72 eutralizing anti-insulin-like growth factor (IGF)-I-receptor antibody inhibited tube formation as wel

73 e kinase activity in the presence of an anti-IGF-I receptor antibody.

74 agens is in part ameliorated by neutralizing IGF-I-receptor antibody.

75 sites of Src-induced phosphorylation of the IGF-I receptor are the same as the ligand-induced autoph

76 otent mitogen for many tumor cell lines, and IGF-I receptors are overexpressed in many tumors.

77 s for the type I insulin-like growth factor (IGF-I) receptor are Shc and insulin receptor substrate (

78 Insulin and insulin-like growth factor-I (IGF-I) receptors are highly homologous tyrosine kinase r

79 ough their cognate tyrosine kinase receptor (IGF-I receptor), are known to play a role in this proces

80 between estrogen receptor (ER)alpha and the IGF-I receptor as a critical mediator of hormone- and gr

81 ncrease in expression of the tyrosine kinase IGF-I receptor, as measured by the amount of both the al

82 omas derived from fibroblasts expressing the IGF-I receptor at high or naturally occurring densities

83 1) We mapped the sites of IGF-I receptor autophosphorylation to peptides represent

84 I-stimulated tyrosine phosphorylation of the IGF-I receptor beta subunit.

85 ng IGF-I type 1 receptor gene expression and IGF-I receptor binding.

86 vival of granule neurons was inhibited by an IGF-I receptor blocking antibody.

87 An IGF-I receptor-blocking antibody inhibited IGF-I-stimula

88 is determined not only by activation of the IGF-I receptor but also by at least three other transmem

89 amino-terminus that bind equally well to the IGF-I receptor but poorly to IGFBPs are as effective as

90 An IGF-I analog with normal affinity for the IGF-I receptor but reduced affinity for IGFBPs evokes a

91 ic actions of IGF-I are mediated through the IGF-I receptor, but how the activation of the IGF-I rece

92 Downregulation of IGF I receptors by antisense phosphorothioate oligonucle

93 hese results suggest that stimulation of the IGF-I receptors by IGF-I or insulin binding stimulates c

94 n family, which become transiently linked to IGF-I receptors by the Grb10 adapter protein following I

95 The insulin-like growth factor type I (IGF-I) receptor can become tyrosine phosphorylated and e

96 ities (1.9 x 10(5) compared with 1.6 x 10(4) IGF-I receptors/cell) in athymic nude mice.

97 Following hormone binding, IGF-I receptors cluster into clathrin-coated pits and ar

98 More importantly, RIP was recruited to the IGF-I receptor complex during IGF-I-induced signaling.

99 owth, serum, liver, and tumor IGF levels and IGF-I receptor concentrations in Caki-I cell membranes w

100 these results indicate that the insulin and IGF-I receptors contribute distinct signals to common do

101 se potency consistent with activation of the IGF-I receptor; death also could be blocked by the prote

102 A mutation in the C terminus of the IGF-I receptor decreased both the rate of receptor inter

103 d in vitro, into R- fibroblasts derived from IGF-I receptor-deficient mice.

104 In contrast, thrombin doubled IGF I receptor density on vascular smooth muscle cells,

105 Antiapoptotic signalling by the IGF-I receptor depended on receptor kinase activity, as

106 In addition, these mutant IGF-I receptors do not affect IGF-I-stimulated p42/p44 m

107 1 or Shc, two of the major substrates of the IGF-I receptor, does not seem sufficiently different to

108 uced, at least in part, by activation of the IGF-I receptor during myoblast differentiation.

109 Overexpression of the IGF-I receptor enabled R- cells to form colonies (27 col

110 Activation of the IGF-I receptor, Erk1/2, p70S6 kinase, and GSK-3beta was

111 In IGF-I receptor-expressing R+ fibroblasts, there is detec

112 Tumor IGF-I receptor expression by immunohistochemistry did no

113 Further, IGF-I receptor expression by the dermal papilla appears

114 ating mitosis; and (b) a reasonable level of IGF-I receptor expression is required for stimulation of

115 Histone-4 transcripts, IGF-I receptor expression, and histochemical staining fo

116 TNF-alpha and IL-1beta act by inhibiting the IGF-I receptor from tyrosine phosphorylating insulin rec

117 asts cultured from the patient had decreased IGF-I-receptor function, as compared with that in contro

118 from mice with homologous disruption of the IGF-I receptor gene) and transfected R- cells expressing

119 ruption of the insulin-like growth factor I (IGF-I) receptor genes, are refractory to transformation

120 We conclude that the endogenous IGF-I receptor has a specific antiapoptotic signalling c

121 d that cells cultured from mice in which the IGF-I receptor has been knocked out by homologous recomb

122 r, excessive activity of the IGF ligands and IGF-I receptor has been suggested as a factor in tumorig

123 ibitors of the insulin-like growth factor-I (IGF-I) receptor have been widely studied for their abili

124 e variants, which bind to IGFBPs but not the IGF-I receptor, have been shown to be potent IGF/IGFBP i

125 hosphorylation, whereas IGF-I activated both IGF-I receptor homodimers and hybrid receptors.

126 Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling has been implicated i

127 Insulin-like growth factor (IGF)-I receptor (IGF-Ir) signaling is required for maint

128 n GD-IgG and the insulin-like growth factor (IGF)-I receptor (IGF-IR).

129 ls in the rat sciatic nerve express both the IGF-I receptor (IGF-I R) and IGF-I throughout postnatal

130 The dynamics of IGF-I receptor (IGF-IR) activation were examined in fres

131 Analysis of IGF-I receptor (IGF-IR) and HGF-SF (c-met) receptor expr

132 tly (p < 0.01) by the catalytically inactive IGF-I receptor (IGF-IR) and the phosphoinositide 3-kinas

133 level of Erk1/2 by 1.2-5.3-fold and that of IGF-I receptor (IGF-IR) by 2-4-fold.

134 e-shift mutation, we have engineered a human IGF-I receptor (IGF-IR) cDNA that produces a receptor 48

135 association of the p85 PI3K subunit with the IGF-I receptor (IGF-IR) effector insulin receptor substr

136 Insulin receptor and IGF-I receptor (IGF-IR) expressions in DRGs and NGF cont

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

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

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

140 d human medulloblastoma cell lines, and that IGF-I receptor (IGF-IR) is constitutively phosphorylated

141 However, if the IGF-I receptor (IGF-IR) is even modestly overexpressed,

142 malignant phenotype, and in lung cancer the IGF-I receptor (IGF-Ir) is often expressed at high level

143 , and recent data have demonstrated that the IGF-I receptor (IGF-IR) is required for in vitro growth

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

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

146 and motile N cells express higher levels of IGF-I receptor (IGF-IR) than less tumorigenic, more adhe

147 development, and differentiation through the IGF-I receptor (IGF-IR) transmembrane tyrosine kinase.

148 In 7 of these, the IGF-I receptor (IGF-IR) was expressed and autophosphoryl

149 Galpha(i) and Gbeta were associated with the IGF-I receptor (IGF-IR), and after ligand stimulation th

150 CRC cells are known to overexpress IGF-I receptor (IGF-IR), c-Met, and uPAR, 3 cell-surface

151 Ob-Rb) and leptin induced phosphorylation of IGF-I receptor (IGF-IR), whereas cotreatment induced syn

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

153 val of multiple cell types by activating the IGF-I receptor (IGF-IR), which signals downstream to a s

154 is through its binding and activation of the IGF-I receptor (IGF-IR).

155 Both the insulin and IGF-I receptors (IGF-IR) are overexpressed in breast can

156 DRG neurons express IGF-I receptors (IGF-IR), and IGF-I activates the phosph

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

158 Truncated IGF-I receptors (IGF-Ir/tf; 482 and 950 amino acids long

159 on in the POA and HYP, are mediated by brain IGF-I receptors (IGF-IRs) in female rats.

160 ivation of the insulin-like growth factor I (IGF-I) receptor (IGF-IR) by its ligand.

161 ential role of insulin-like growth factor I (IGF-I) receptor (IGF-IR) in cell proliferation by overex

162 y tissues, the insulin-like growth factor I (IGF-I) receptor (IGF-IR) is known to functionally oppose

163 The insulin-like growth factor I (IGF-I) receptor (IGF-IR) is known to regulate a variety

164 nd the related insulin-like growth factor-I (IGF-I) receptor (IGF-IR) mediate a variety of metabolic

165 receptor (IR), insulin-like growth factor-I (IGF-I) receptor (IGF-IR), and nerve growth factor recept

166 r (IR) and the insulin-like growth factor I (IGF-I) receptor (IGF-IR).

167 of the type 1 insulin-like growth factor I [IGF-I] receptor [IGF-IR]) do not express insulin recepto

168 (IRS) isoforms to transduce signals from the IGF-I receptor, IGF-I has the same relative effect on th

169 In FL5.12 cells transfected with wild-type IGF-I receptors, IGF-I affords protection from interleuk

170 tions, Grb10 was essentially undetectable in IGF-I receptor immunoprecipitates from stimulated R+ cel

171 Expression of a human IGF-I receptor in 32D/IRS-1 cells also results in nuclea

172 dependent manner the expression of IGF-I and IGF-I receptor in both the intima and the adventitia.

173 To determine the role of the IGF-I receptor in load-induced skeletal muscle hypertrop

174 that details the expression of IGF-I and the IGF-I receptor in sections of human skin is needed.

175 action in the liver and that deletion of the IGF-I receptor in skeletal muscle results in severe insu

176 can bypass the requirement for a functional IGF-I receptor in the full transformation of mouse embry

177 tflow pathway, the expression of IGFBP-5 and IGF-I receptor in the TM was characterized.

178 fluid from nephrotic rats autophosphorylates IGF-I receptors in cultured proximal tubular cells.

179 10 interacts preferentially with insulin vs. IGF-I receptors in intact cells and, thus, may have a ro

180 se is a pleiotropic feature of both IL-3 and IGF-I receptors in myeloid progenitors, prevention of ap

181 tion of both the epidermal growth factor and IGF-I receptors in response to TPA treatment in LID mice

182 As there is a paucity of IGF-I receptors in the liver and as the IGF-IGFBP system

183 reductions in phosphorylation of insulin and IGF-I receptors in transformed mammary tissue.

184 d that 14-3-3sigma is a positive mediator of IGF-I receptor-induced cell proliferation.

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

186 IGF-I receptor inhibition prevents rapamycin-induced Akt

187 actor I (IGF-I) signaling pathway, including IGF-I receptor, insulin receptor substrate 1, and phosph

188 In parallel, IGF-I activates IGF-I receptor, insulin receptor substrate-1 (IRS-1), ph

189 The physiological relevance of the decorin/IGF-I receptor interaction was corroborated in two anima

190 Low temperature (15 degrees C) decreased IGF-I receptor internalization and completely inhibited

191 study investigates the relationship between IGF-I receptor internalization and signaling via IRS-1 a

192 d protein kinase pathway activation requires IGF-I receptor internalization, whereas the IRS-1 pathwa

193 ever, for the major substrate of the insulin/IGF-I receptor (IRS-1) despite the well known interactio

194 orylation of Akt, whereas phosphorylation of IGF-I receptor, IRS1/2 and p44/42 mitogen-activated prot

195 and Balb/c3T3 fibroblasts and in neurons the IGF-I receptor is coupled to an inhibitory G protein, G(

196 ceptor and the insulin-like growth factor I (IGF-I) receptor is mediated by the SH2 domain, and we sh

197 dence that the insulin-like growth factor-I (IGF-I) receptor is required for transformation by a vari

198 An IGF-I receptor lacking a functional ATP binding site pro

199 GF-I receptor, but how the activation of the IGF-I receptor leads to these biological responses is po

200 decrease in the insulin-like growth factor (IGF)-I receptor levels leading to a reduced IGF-I-mediat

201 blocking the AKT pathway and by reducing the IGF-I receptor levels in mammary gland.

202 els compared with nonlesional areas, whereas IGF-I receptor levels were equivalent--conditions for en

203 o abnormalities in the function or number of IGF-I receptors may also retard intrauterine and subsequ

204 fferent roles in insulin-like growth factor (IGF)-I receptor-mediated signal transduction.

205 Consistent with this, an in vivo marker of IGF-I receptor-mediated action was increased 10-fold in

206 le cells is up-regulated by IGF-I through an IGF-I receptor-mediated mechanism.

207 r blocking alphaVbeta3 occupancy could alter IGF-I receptor-mediated signal transduction, the ability

208 ults suggest that IRS-4 is implicated in the IGF-I receptor mitogenic signaling pathway.

209 Dominant-negative muscle-specific IGF-I receptor (MKR) mice exhibit elevated lipid levels

210 growth factor (IGF)-I signaling through the IGF-I receptor modulates cellular adhesion and prolifera

211 IGF-I binding and IGF-I receptor mRNA concentrations in porcine granulosa

212 increase in glomerular TGF-beta, Smad3, and IGF-I receptor mRNA expression compared with the NS grou

213 The IGF-I receptor mRNA in the lung was increased by 200% (p

214 ng a series of insulin-like growth factor I (IGF-I) receptor mutants, we have attempted to define dom

215 ls, but not their differentiating cells, are IGF-I receptor negative.

216 ibroblast cell lines each from wild-type and IGF-I receptor null embryos (R-).

217 We conclude that late passage IGF-I receptor null mouse embryo fibroblasts can be tran

218 done in mouse fibroblasts overexpressing the IGF-I receptor (NWTb3) with the porcine IGFRE (three rep

219 tors, the effect of IFNgamma on SCF, EP, and IGF-I receptors of human erythroid progenitor cells has

220 ogenic activities through stimulation of the IGF-I receptor on the cell surface.

221 ation (Arg59stop) that reduced the number of IGF-I receptors on fibroblasts.

222 n binds to the insulin-like growth factor-I (IGF-I) receptor on endothelial cells with an affinity in

223 Antagonists of the IGF-I receptor or alphaVbeta3 integrin reversed these ch

224 yoblasts by IGF analogues that activated the IGF-I receptor or by unrelated growth factors such as pl

225 revented by IGF analogues that activated the IGF-I receptor or by unrelated growth factors such as pl

226 eceptor or the insulin-like growth factor I (IGF-I) receptor, or both.

227 ese data demonstrate that a functional IGF I-IGF I receptor pathway is essential for thrombin-induced

228 numbers of SCF and EP receptors, but not of IGF-I receptors, per ECFC, calculated by Scatchard analy

229 g production of IGF-II and activation of the IGF-I receptor, phosphatidylinositol 3-kinase, and Akt i

230 growth factor I (IGF-I) that consists of the IGF-I receptor, phosphoinositide 3-kinase (PI3 kinase),

231 Decorin addition causes IGF-I receptor phosphorylation and activation, which is

232 account for the increase in the duration of IGF-I receptor phosphorylation and for enhanced downstre

233 the addition of 10 nM IGF-I, whereas maximal IGF-I receptor phosphorylation occurred within 5 min.

234 Basal IGF-I receptor phosphorylation was increased 320% in str

235 IGF-I receptor and regulates the duration of IGF-I receptor phosphorylation.

236 These findings indicate the existence of an IGF-I receptor-PI 3-kinase-caspase 3 pathway in cardiomy

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

238 ning for alpha-actin, growth factors (IGF-I, IGF-I receptor, platelet-derived growth factor-BB, and b

239 Insulin-like growth factor-I (IGF-I) receptor plays an important role in normal cell c

240 l basal keratinocytes are IGF-I negative but IGF-I receptor positive, and (iii) the keratinocytes of

241 ransient binding of both Grb10 and GIGYF1 to IGF-I receptors, presumably via the adapter function of

242 EP/pSFFV cells with IGF-I or transfection of IGF-I receptor prevents these changes.

243 isolated from S/Pla mice had an increase of IGF-I receptor protein, and IGF-I stimulated a TGF-beta

244 ing either insulin receptors (R-IR cells) or IGF-I receptors (R+ cells) were used to investigate the

245 und to immobilized recombinant soluble human IGF-I receptor, recombinant human IGF-binding protein 1,

246 studies demonstrate that the domains of the IGF-I receptor required for its antiapoptotic function a

247 ke growth factor I (IGF-I) activation of the IGF-I receptor rescues SH-SY5Y human neuroblastoma cells

248 experiments indicate that TNF-alpha promotes IGF-I receptor resistance in neurons and inhibits the ab

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

250 nity for IGFBP-5 but normal affinity for the IGF-I receptor, showing the highest potency.

251 To study the role of IGF-I receptor signaling on cell cycle events we utilize

252 To further investigate the IGF-I receptor signaling pathways that are required for

253 he IGF-I receptor and that activation of the IGF-I receptor signaling pathways, although not essentia

254 (IGFBP-3) and -4, the negative regulators of IGF-I receptor signaling, contributes to the resistance

255 ile both proteins are substrates involved in IGF-I receptor signaling, they apparently demonstrate im

256 proteins may also play a regulatory role in IGF-I receptor signaling.

257 ppaB and JNK activation, plays a key role in IGF-I receptor signaling.

258 gma protein in insulin-like growth factor-I (IGF-I) receptor signaling.

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

260 MKR mice, which express a dominant negative IGF-I receptor specifically in skeletal muscle, have mar

261 del (MKR) that expresses a dominant negative IGF-I receptor specifically in skeletal muscle.

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

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

264 enabled by IGF analogues that activated the IGF-I receptor; survival was dependent on stimulation of

265 ion of the exact pathways emanating from the IGF-I receptor that are involved in mediating these sign

266 Following activation of the IGF-I receptor, the mitogen-activated protein kinase and

267 sts expressing tyrosine 1250 and 1251 mutant IGF-I receptors, the signal transduction pathways impact

268 IGF-II that prevent them from activating the IGF-I receptor to stimulate cell survival and proliferat

269 e in neurons and inhibits the ability of the IGF-I receptor to tyrosine-phosphorylate the IRS-2 docki

270 may serve to positively link the insulin and IGF-I receptors to an uncharacterized mitogenic signalin

271 In the C terminus of the IGF-I receptor, two mutations, one at tyrosine 1251 and

272 In contrast, IGF-I receptor tyrosine kinase activity was not increase

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

274 ably, IL-1beta suppresses the ability of the IGF-I receptor tyrosine kinase to phosphorylate its majo

275 y facilitating interaction of IGF-I with the IGF-I receptor tyrosine kinase.

276 that occurred independently of IGF-I and the IGF-I receptor tyrosine kinase.

277 null mice exhibit decreased IGF-I-stimulated IGF-I receptor tyrosine phosphorylation and augmented ER

278 FAK, paxillin, and IGF-I receptor tyrosine phosphorylation had similar conc

279 IGF-I elicited IGF-I receptor tyrosine phosphorylation, resulting in th

280 of insulin and insulin-like growth factor-I (IGF-I) receptor tyrosine kinase activity, and this prote

281 Thus, it appears that signaling from the IGF-I receptor utilizes two distinct pathways leading ei

282 ouse embryo cells with a wild-type number of IGF-I receptors (W cells).

283 In addition, the IGF-I receptor was expressed by the TM and showed cell-s

284 alterations in receptor kinase activity, the IGF-I receptor was immunoprecipitated and then analyzed

285 The antiapoptotic capacity of the IGF-I receptor was not shared by other growth factors te

286 In both models the IGF-I receptor was up-regulated in decorin-deficient mic

287 specific to the insulin receptor (IR) or the IGF-I receptor, we have generated brown preadipocyte cel

288 IGFBP-5 and IGF-I receptor were expressed at significant levels by T

289 rosarcomas expressing parental levels of the IGF-I receptor were not affected by rhIGF-I therapy.

290 ast cancer cell lines, whereas IRS-1 and the IGF-I receptor were not induced.

291 Insulin and IGF-I receptors were detected in smooth-muscle cells and

292 However, when IGF-I receptors were overexpressed in a Rat-1 background

293 or the SCF and EP receptors, but not for the IGF-I receptors, were decreased by 50% to 60% after 3 ho

294 are rat hippocampal cells expressing a human IGF-I receptor, which differentiate to a neuronal phenot

295 Blockade of the IGF-I receptor with a neutralizing antibody abrogated th