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 on-glycosylated forms display more efficient IGF-I receptor activation in vitro, suggesting that the

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

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

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

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

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

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

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

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

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

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

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

46 I signaling by increasing phosphorylation of IGF-I receptor and its downstream effector AKT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 97 kDa, representing the beta-subunit of the IGF-I receptor, and a predominant tyrosyl-phosphorylated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Downregulation of IGF I receptors by antisense phosphorothioate oligonucle

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 1 or Shc, two of the major substrates of the IGF-I receptor, does not seem sufficiently different to

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

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

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

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

114 Tumor IGF-I receptor expression by immunohistochemistry did no

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 evoked by astrocytic activation through its IGF-I receptors (IGF-IRs).

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

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

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

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

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

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

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

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

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

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

173 naling and phosphorylation/activation of the IGF-I receptor (IGF1R).

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

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

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

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

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

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

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

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

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

183 10 interacts preferentially with insulin vs. IGF-I receptors in intact cells and, thus, may have a ro

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

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

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

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

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

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

190 IGF-I receptor inhibition prevents rapamycin-induced Akt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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