ライフサイエンスコーパス: insulin receptor substrate-1

1 e a requirement of Rab5 in presenting p85 to insulin receptor substrate 1.

2 proliferating cell nuclear antigen, and the insulin receptor substrate 1.

3 ion of the IGF-I/insulin hybrid receptor and insulin receptor substrate 1.

4 r and Akt as well as decreased expression of insulin receptor substrate 1.

5 stance through inhibitory phosphorylation of insulin receptor substrate 1.

6 prevailing model of S6K1 phosphorylation of insulin receptor substrate-1.

7 including sites on the insulin receptor and insulin receptor substrate-1.

8 operative in the presence or absence of the insulin receptor substrate-1.

9 sm that may involve its association with the insulin receptor substrate-1.

10 f the mTOR complex 1-dependent regulation of insulin receptor substrate-1.

11 TNF-alpha-mediated serine phosphorylation of insulin receptor substrate-1.

12 that PKC activation differentially inhibited insulin receptor substrate 1/2 (IRS1/2) signaling of ins

13 as evidenced by increased phosphorylation of insulin receptor substrate 1/2 and enhanced ERK/Akt acti

14 inding domain-containing proteins, including insulin receptor substrate 1/2, Shc, and IL-4R interacti

15 -induced phosphorylation of Akt, ERK1/2, and insulin receptor substrate-1/2 was decreased and followe

16 ermined the kinetics of dephosphorylation of insulin receptor substrate-1/2, Akt, and ERK1/2, phospho

17 and phosphoinositide 3-kinase decreased, and insulin receptor substrate-1 307 phosphorylation increas

18 sduction by impairing the phosphorylation of insulin receptor substrate 1, a protein that couples act

19 ion was largely dependent on the presence of insulin receptor substrate-1, a major substrate of the I

20 884614, OR=2.44, CI=1.42-4.48, P=0.002), and insulin receptor substrate 1 AA+AG (rs1801278, OR=2.71,

21 e insulin sensitivity coincided with reduced insulin receptor substrate-1 abundance in skeletal muscl

22 We showed that MEMO1 binds to insulin receptor substrate 1, activates the downstream P

23 ted with increased insulin receptor beta and insulin receptor substrate 1 activation along with activ

24 Here, we show that insulin receptor substrate 1 and 2 (IRS1/2) cooperate wi

25 a mouse model that harbors hepatic-specific insulin receptor substrate 1 and 2 deletions (double kno

26 c modification of several proteins including insulin receptor substrate 1 and beta-catenin, two impor

27 port a non-canonical interaction between the insulin receptor substrate 1 and certain oncogenic varia

28 e, with dramatically decreased expression of insulin receptor substrate 1 and glucose transporter 4 i

29 on both of its downstream docking proteins, insulin receptor substrate 1 and insulin receptor substr

30 tenuates insulin signaling and expression of insulin receptor substrate 1 and phosphoinositide 3-kina

31 uced tumors showed upregulated expression of insulin receptor substrate 1 and phosphorylated forms of

32 because of the impaired interaction between insulin receptor substrate 1 and the p85alpha subunit of

33 Insulin receptor substrate-1 and -2 (IRS-1 and IRS-2), t

34 failed to phosphorylate the adaptor proteins insulin receptor substrate-1 and -2 in response to IGF-I

35 Insulin receptor substrate-1 and -2 phosphorylation and

36 timulate glucose transport and phosphorylate Insulin receptor substrate-1 and Akt.

37 nd JNK1/2) was unchanged, but expressions of insulin receptor substrate-1 and Grb2-associated binder-

38 Absence of LAR enhanced phosphorylation of insulin receptor substrate-1 and insulin receptor substr

39 sphatidylinositol 3-kinase (PI3K) binding to insulin receptor substrate-1 and insulin receptor substr

40 In adipose, endotoxemia suppressed insulin receptor substrate-1 and markedly induced suppre

41 ling and known feedback mechanisms affecting insulin receptor substrate-1 and phosphatidylinositol 3-

42 ially the endoplasmic reticulum, mediated by insulin receptor substrate-1 and phosphatidylinositol 3-

43 TNF-alpha-mediated serine phosphorylation of insulin receptor substrate-1 and protein tyrosine phosph

44 TrkB receptor and involves docking proteins insulin receptor substrate-1 and Shc, which convey recep

45 Fc blocked IGF-I mediated phosphorylation of insulin receptor substrate-1 and subsequent extracellula

46 lones gain copy number amplifications of the insulin receptor substrate-1 and substrate-2 (IRS1 or IR

47 it with the IGF-I receptor (IGF-IR) effector insulin receptor substrate-1 and with ErbB3, implicating

48 cing a negative feedback signal that targets insulin receptor substrates 1 and 2 (IRS1 and -2).

49 stance is a hallmark of type 2 diabetes, and insulin receptor substrates 1 and 2 (IRS1 and IRS2) are

50 Foxo1 signaling, which can be independent of insulin receptor substrates 1 and 2 (Irs1 and Irs2), rev

51 Insulin receptor substrates 1 and 2 (IRS1/2) mediate mit

52 phosphorylation of the insulin receptor and insulin receptor substrates 1 and 2 are elevated.

53 The association of insulin receptor substrates 1 and 2 with alphap85 subuni

54 f the levels and subcellular distribution of insulin receptor substrates 1 and 2, the p85alpha subuni

55 ation by 60% and tyrosine phosphorylation of insulin receptor substrates-1 and -2 by 60 and 40%, resp

56 ays: one mediated by STAT6, and the other by insulin receptor substrates-1 and -2 via activation of P

57 insulin signaling through phosphorylation of insulin-receptor substrates 1 and 2 at sites that interf

58 egulin, and glucose metabolism-involved gene insulin receptor substrate 1), and 27 genes in the nondi

59 es and, in some cells, reduced expression of insulin receptor substrate 1, and both IGF1 and insulin

60 ta-catenin, c/EBPalpha,c-Myc, cyclin D1, and insulin receptor substrate 1, and cell growth/survival.

61 lation levels of IL-4Ralpha, Janus kinase 1, insulin receptor substrate 1, and insulin receptor subst

62 signaling pathway, including IGF-I receptor, insulin receptor substrate 1, and phosphatidylinositol 3

63 sine phosphorylation of the hybrid receptor, insulin receptor substrate 1, and the glycogen synthesis

64 syl phosphorylation of the insulin receptor, insulin receptor substrate 1, and their downstream casca

65 significant increases in glucose metabolism, insulin receptor substrate-1, and Akt activity in muscle

66 Skeletal muscle insulin receptor, insulin receptor substrate-1, and Akt contents were unch

67 insulin-signaling pathway (insulin receptor, insulin receptor substrate-1, and Akt).

68 and down-regulation of the insulin receptor, insulin receptor substrate-1, and GLUT4.

69 nase, enhances the serine phosphorylation of insulin receptor substrate-1, and increases the expressi

70 ylation of insulin receptor beta subunit and insulin receptor substrate-1, and serine phosphorylation

71 e phosphorylation of the insulin receptor or insulin receptor substrate-1, and without enhancing phos

72 us (DH) for deletion of insulin receptor and insulin receptor substrate-1 are lean, insulin resistant

73 This identifies insulin receptor substrate-1 as a novel nonreceptor targ

74 insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 as well as Akt phosphorylat

75 confined to signaling pathways that include insulin receptor substrate-1, as the alpha(1)-adrenergic

76 sulin stimulation (approximately 20-fold) of insulin receptor substrate 1-associated phosphatidylinos

77 in skeletal muscle and insulin activation of insulin receptor substrate-1-associated phosphatidylinos

78 rylation of insulin receptor substrate-1 and insulin receptor substrate-1-associated phosphoinositide

79 ed protein kinase (AMPK), and phosphorylated insulin receptor substrate 1 at serine 307 (IRS1-s307).

80 The insulin-like growth factor I/insulin receptor substrate 1 axis controls, in a nonredu

81 also exhibited increased binding to phospho-insulin receptor substrate-1 by 41% and 83%, respectivel

82 ozygous deletion of the insulin receptor and insulin receptor substrate-1 (DH) or the obese, hypergly

83 correlated with enhanced phosphorylation of insulin receptor substrate 1, effects that were both blo

84 We now show that mTOR inhibition induces insulin receptor substrate-1 expression and abrogates fe

85 effects including an mTOR-dependent loss in insulin receptor substrate-1 expression leading to feedb

86 sen, an antisense oligonucleotide preventing insulin receptor substrate-1 expression, inhibited corne

87 In an insulin receptor substrate-1 gene disrupted beta-cell tu

88 found greater inhibitory phosphorylation of insulin receptor substrate 1 in each brain region examin

89 2 interacts with and directly phosphorylates insulin receptor substrate-1 in cardiomyocytes, causing

90 phosphorylation of the insulin receptor and insulin receptor substrate-1 in response to insulin incr

91 t autophosphorylation and phosphorylation of insulin receptor substrate-1 in vivo and could be cross-

92 to phosphorylate its major docking protein, insulin receptor substrate-1, in MCF-7 breast carcinoma

93 y 29% +/- 13% and phosphorylation of Akt and insulin receptor substrate 1 increased by 35% +/- 9% and

94 Both downregulation of insulin receptor substrate 1 (IRS-1) and dominant-negati

95 Insulin receptor substrate 1 (IRS-1) and IRS-2 are cytop

96 We identified insulin receptor substrate 1 (IRS-1) and IRS-2 as signal

97 ults in reduced levels of insulin-stimulated insulin receptor substrate 1 (IRS-1) and phosphotyrosine

98 nied by a decrease in the phosphorylation of insulin receptor substrate 1 (IRS-1) and the association

99 ta-arrestin-1 is involved in insulin-induced insulin receptor substrate 1 (IRS-1) degradation.

100 Furthermore, we showed that the insulin receptor substrate 1 (IRS-1) expression and insu

101 salicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated wi

102 phosphorylation of the insulin receptor and insulin receptor substrate 1 (IRS-1) in muscle of transg

103 Insulin receptor substrate 1 (IRS-1) is a critical adapt

104 Insulin receptor substrate 1 (IRS-1) is a major signalin

105 Insulin receptor substrate 1 (IRS-1) is a major substrat

106 Insulin receptor substrate 1 (IRS-1) is the major signal

107 that JNK phosphorylates the adapter protein insulin receptor substrate 1 (IRS-1) on Ser 307 and inhi

108 I [IGF-I] receptor [IGF-IR]) do not express insulin receptor substrate 1 (IRS-1) or IRS-2.

109 Furthermore, the expression of insulin receptor substrate 1 (IRS-1) phosphorylated at s

110 Insulin increased AKT and insulin receptor substrate 1 (IRS-1) phosphorylation, sy

111 Insulin receptor substrate 1 (IRS-1) plays a key role in

112 Insulin receptor substrate 1 (IRS-1) plays an important

113 ation factor 4E (eIF4E) S209, Smad2 S465/67, insulin receptor substrate 1 (IRS-1) S612, mitogen-activ

114 egative feedback loop imposed on the IGF-IR- insulin receptor substrate 1 (IRS-1) signaling complex,

115 We have previously shown that insulin receptor substrate 1 (IRS-1) translocates to the

116 (SOCS3) show lower phosphorylation levels of insulin receptor substrate 1 (IRS-1) Tyr(896) and Akt Se

117 Similarly, the docking protein insulin receptor substrate 1 (IRS-1) was down-regulated

118 In this report, we identified insulin receptor substrate 1 (IRS-1), a critical mediato

119 th decreased levels of serine-phosphorylated insulin receptor substrate 1 (IRS-1), a molecule implica

120 estradiol (E2) upregulates the expression of insulin receptor substrate 1 (IRS-1), a molecule transmi

121 Phosphorylation of insulin receptor substrate 1 (IRS-1), activation of IRS-

122 ylation of JNK and serine phosphorylation of insulin receptor substrate 1 (IRS-1), along with inhibit

123 -1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdow

124 ng proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase

125 ling (SOCS3) in muscle, which led to loss of insulin receptor substrate 1 (IRS-1), thereby impairing

126 pogenesis, we examined the effect of BMP7 in insulin receptor substrate 1 (IRS-1)-deficient brown pre

127 We have previously characterized an insulin receptor substrate 1 (IRS-1)-overexpressing beta

128 in spite of decreased signaling through the insulin receptor substrate 1 (IRS-1)-phosphoinositide (P

129 (IGF-I) signal through the scaffold protein insulin receptor substrate 1 (IRS-1).

130 n receptor substrates (IRS), one of which is insulin receptor substrate 1 (IRS-1).

131 et of rapamycin)-mediated phosphorylation of insulin receptor substrate 1 (IRS-1).

132 d51 and the major IGF-IR signaling molecule, insulin receptor substrate 1 (IRS-1).

133 ptor (IR) and its substrate proteins such as insulin receptor substrate 1 (IRS-1).

134 Insulin-stimulated phosphorylation of insulin receptor substrate-1 (IRS-1) and -2, and Akt was

135 owed that E2 influenced on protein levels of insulin receptor substrate-1 (IRS-1) and impaired insuli

136 ugh both proteasome-dependent degradation of insulin receptor substrate-1 (IRS-1) and inhibition of t

137 sulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associate

138 owing to the deletion of the genes encoding insulin receptor substrate-1 (Irs-1) and Irs-2 (referred

139 IGF-1 stimulates tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-2 and their

140 Insulin receptor substrate-1 (IRS-1) and IRS-2 are known

141 Although insulin receptor substrate-1 (IRS-1) and IRS-2, among ot

142 igands for ALK and that upon ALK activation, insulin receptor substrate-1 (IRS-1) and other substrate

143 stimulated tyrosyl phosphorylation of IR and insulin receptor substrate-1 (IRS-1) and phosphoinositid

144 We assessed the roles of insulin receptor substrate-1 (IRS-1) and Shc in insulin

145 In the present study, we identified insulin receptor substrate-1 (IRS-1) as a novel substrat

146 ylation of c-Jun N-terminal kinase (JNK) and insulin receptor substrate-1 (IRS-1) at Ser-307 were inc

147 I) 3-kinase/Akt signaling by phosphorylating insulin receptor substrate-1 (IRS-1) at Ser-636/639.

148 Tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) by the insulin rece

149 Serine phosphorylation of insulin receptor substrate-1 (IRS-1) can regulate tyrosi

150 We have shown previously that insulin receptor substrate-1 (IRS-1) can translocate to

151 n-like growth factor-I receptor (IGF-IR) and insulin receptor substrate-1 (IRS-1) expression, two key

152 ke growth factor receptor (IGF-IR) or of the insulin receptor substrate-1 (IRS-1) genes in animals ca

153 e also report increased concentration of the insulin receptor substrate-1 (IRS-1) in L1CAM(+) exosome

154 wth factor I (IGF-I) regulates the levels of insulin receptor substrate-1 (IRS-1) in prostate epithel

155 activity of PI3K/protein kinase B (AKT) and insulin receptor substrate-1 (IRS-1) in the hypothalamic

156 Serine phosphorylation of insulin receptor substrate-1 (IRS-1) inhibits insulin si

157 The insulin receptor substrate-1 (IRS-1) is a docking protei

158 Ser/Thr phosphorylation of insulin receptor substrate-1 (IRS-1) is a negative regul

159 Insulin receptor substrate-1 (IRS-1) is a signaling adap

160 The insulin receptor substrate-1 (IRS-1) is one of the major

161 ses a route that promotes phosphorylation of insulin receptor substrate-1 (IRS-1) on Tyr(989), a cano

162 h factor (IGF-I) receptor and do not express insulin receptor substrate-1 (IRS-1) or IRS-2.

163 EFs and several other cell lines requires an insulin receptor substrate-1 (IRS-1) phosphorylated on t

164 In addition, insulin receptor substrate-1 (IRS-1) phosphorylation and

165 he duration of IGF-I-stimulated receptor and insulin receptor substrate-1 (IRS-1) phosphorylation.

166 Insulin receptor substrate-1 (IRS-1) plays a central rol

167 The pleckstrin homology (PH) domain of the insulin receptor substrate-1 (IRS-1) plays a role in dir

168 Our studies revealed that insulin receptor substrate-1 (IRS-1) protein levels decr

169 showed that IGF-I, IGF-IR mRNAs, and phospho-insulin receptor substrate-1 (IRS-1) protein were decrea

170 decreased insulin signaling at the level of insulin receptor substrate-1 (IRS-1) tyrosine phosphoryl

171 In fact, Ad-36 decreased insulin receptor substrate-1 (IRS-1) tyrosine phosphoryl

172 of IGF-I-induced cell cycle progression and insulin receptor substrate-1 (IRS-1) tyrosine phosphoryl

173 ulin-dependent receptor autophosphorylation, insulin receptor substrate-1 (IRS-1) tyrosine phosphoryl

174 These effects are mediated by insulin receptor substrate-1 (IRS-1) via the mitogen-act

175 phoinositide-3 kinase (PI3K) associated with insulin receptor substrate-1 (IRS-1) was attenuated (P <

176 The insulin receptor substrate-1 (IRS-1), a docking protein

177 a-catenin binds to and co-localizes with the insulin receptor substrate-1 (IRS-1), a docking protein

178 most commonly detected polymorphism in human insulin receptor substrate-1 (IRS-1), a glycine to argin

179 suppressor gene PTEN and do not express the insulin receptor substrate-1 (IRS-1), a major substrate

180 phosphorylation of the insulin receptor and insulin receptor substrate-1 (IRS-1), and it reduces pho

181 hosphorylated IRbeta, tyrosyl-phosphorylated insulin receptor substrate-1 (IRS-1), and p85-associated

182 lation of the IGF-1R beta subunit, the EGFR, insulin receptor substrate-1 (IRS-1), and the Shc adapte

183 During insulin or NGF stimulation TrkA, insulin receptor substrate-1 (IRS-1), INSR (and presumab

184 tyrosine phosphorylation of the receptor and insulin receptor substrate-1 (IRS-1), leading to activat

185 ve the phosphorylation of serine residues in insulin receptor substrate-1 (IRS-1), leading to impairm

186 ith cardiac hypertrophy and stress including insulin receptor substrate-1 (IRS-1), phosphatidyl inosi

187 In parallel, IGF-I activates IGF-I receptor, insulin receptor substrate-1 (IRS-1), phosphatidylinosit

188 The signaling protein insulin receptor substrate-1 (IRS-1), shown here to be a

189 cadherin function via loss of expression of insulin receptor substrate-1 (IRS-1), the principal IGF1

190 -high cells, and this enhanced expression of insulin receptor substrate-1 (IRS-1), the principle intr

191 effects of Pes1 are similar to those of the insulin receptor substrate-1 (IRS-1), we investigated th

192 BT-20 cells do not express insulin receptor substrate-1 (IRS-1), which is known to

193 tal muscle by blocking insulin activation of insulin receptor substrate-1 (IRS-1)-associated phosphat

194 Neither treatment had any effect on basal insulin receptor substrate-1 (IRS-1)-associated PI 3-kin

195 ation and degradation of the adaptor protein insulin receptor substrate-1 (IRS-1).

196 ns increases Ser(312) phosphorylation of the insulin receptor substrate-1 (IRS-1).

197 ieving S6K1-dependent negative regulation of insulin receptor substrate-1 (IRS-1).

198 NK) and subsequent serine phosphorylation of insulin receptor substrate-1 (IRS-1).

199 f key insulin signalling proteins, including insulin receptor substrate-1 (IRS-1).

200 d increase in ROK-alpha association with the insulin receptor substrate-1 (IRS-1).

201 ndent murine hemopoietic cell line devoid of insulin receptor substrate-1 (IRS-1).

202 of postinsulin receptor substrates, such as insulin receptor substrate-1 (IRS-1).

203 olling ROCK-dependent phosphorylation of the insulin receptor substrate-1 (IRS-1).

204 o regulate insulin signaling at the level of insulin receptor substrate-1 (IRS-1).

205 rtment within tumor cells, where it degraded insulin receptor substrate-1 (IRS-1).

206 ced phosphorylation of insulin receptor (IR)/insulin receptor substrate-1 (IRS-1)/Akt pathway in the

207 Activation of the insulin (IN)/insulin receptor substrate-1 (IRS-1)/mitogen-associated

208 lin receptor; 2) tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1); 3) association of

209 integrin forms a complex with the IGF-IR and insulin receptor substrate-1 (IRS-1); this complex does

210 within the phosphotyrosine-binding domain of insulin receptor substrate-1 (IRS-PTB), we have used NMR

211 the levels of the IGF-IR and its substrate, insulin-receptor substrate 1 (IRS-1), are often elevated

212 s associated with reduced insulin-stimulated insulin receptor substrate 1- (IRS-1-) and IRS-2-associa

213 e peptides (dilp2-3,5(-/-)) and mice lacking insulin receptor substrate 1 (Irs1(-/-)), and two indepe

214 KD cells reduced tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) (pY(896)) and phosph

215 sistance because of enhanced skeletal muscle insulin receptor substrate 1 (IRS1) and Akt phosphorylat

216 inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt.

217 d fat, including tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) and IRS2 and activat

218 ion of the PI 3-kinase pathway by recruiting insulin receptor substrate 1 (IRS1) and IRS2 in response

219 These effects are mediated by insulin receptor substrate 1 (IRS1) and IRS2, which also

220 The insulin-signaling pathway requires insulin receptor substrate 1 (IRS1) and IRS2, which are

221 is critical for the membrane recruitment of insulin receptor substrate 1 (IRS1) and signal transmiss

222 nsulin resistance by increase in Ser(P)(307)-insulin receptor substrate 1 (IRS1) and subsequent decli

223 At 32 weeks, lower insulin receptor substrate 1 (IRS1) at S636/639 and Akt

224 by stimulating phosphorylation of rat/mouse insulin receptor substrate 1 (Irs1) at Ser(307) (Ser(312

225 ase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307.

226 r insulin-dependent association of PI3K with insulin receptor substrate 1 (IRS1) but abbreviated Akt

227 based gene expression profiling we found the insulin receptor substrate 1 (IRS1) gene as one of the m

228 Common genetic variants in the insulin receptor substrate 1 (IRS1) gene have been recen

229 lele of rs2943641 near the gene encoding for insulin receptor substrate 1 (IRS1) has been associated

230 Mechanistically, insulin receptor substrate 1 (Irs1) is a direct target o

231 Insulin receptor substrate 1 (IRS1) is a key mediator of

232 e reverse-phase protein array, we found that insulin receptor substrate 1 (IRS1) is the most highly u

233 ion against insulin resistance by increasing insulin receptor substrate 1 (IRS1) levels.

234 kinase A (PKA)-dependent phosphorylation of insulin receptor substrate 1 (IRS1) on tyrosine residues

235 known node of PI3K inhibition and decreased insulin receptor substrate 1 (IRS1) protein levels.

236 SHH-treated CGNPs showed increased levels of insulin receptor substrate 1 (IRS1) protein, which was a

237 that has been shown to specifically degrade insulin receptor substrate 1 (IRS1) protein.

238 dent receptor autophosphorylation as well as insulin receptor substrate 1 (IRS1) tyrosine phosphoryla

239 Insulin receptor substrate 1 (IRS1) was overexpressed in

240 ndent proteolysis of the CRL7 target protein insulin receptor substrate 1 (IRS1), a component of the

241 insulin-induced tyrosine phosphorylation of insulin receptor substrate 1 (IRS1), activation of prote

242 o trigger multisite seryl phosphorylation of insulin receptor substrate 1 (IRS1), leading to its ubiq

243 LKB1 deletion markedly reduced the levels of insulin receptor substrate 1 (IRS1), peroxisome prolifer

244 PI3K; thus, we examined the requirement for insulin receptor substrate 1 (IRS1), which binds and act

245 JNK-dependent proteasomal degradation of the insulin receptor substrate 1 (IRS1), which in turn inhib

246 h "feedback" phosphorylation of the upstream insulin receptor substrate 1 (IRS1).

247 MiR-487b is predicted to target insulin receptor substrate 1 (IRS1).

248 involves ubiquitin-dependent degradation of insulin receptor substrate 1 (IRS1).

249 -growth factor-1 signaling pathways, such as insulin receptor substrate-1 (IRS1) and IRS2, differenti

250 ide explained by attenuation of an mTORC1-to-insulin receptor substrate-1 (IRS1) feedback and reduced

251 gous deletion of the Insulin receptor and/or insulin receptor substrate-1 (IRS1) genes.

252 The insulin receptor substrate-1 (IRS1) is a critical elemen

253 Brain insulin receptor substrate-1 (IRS1) phosphorylation (pS(

254 The gene encoding insulin receptor substrate-1 (IRS1) represents a strong

255 KO MEFs displayed reduced protein content of insulin receptor substrate-1 (IRS1), pivotal to insulin

256 Female mice haploinsufficient for insulin receptor substrate-1 (IRS1-het) are hyperinsulin

257 use aortic smooth muscle cells isolated from insulin receptor substrate -1 knockout (IRS-1-/-) mice t

258 eficient in cyclin D2 (D2KO) with either the insulin receptor substrate 1 knockout (IRS1KO) mice or t

259 , glycogen synthase, and protein kinase B or insulin receptor substrate-1 level was unchanged.

260 Akt, FoxO1, and c-Src, but did not activate insulin receptor substrate-1-like insulin.

261 o insulin action, and 3) basal inhibition of insulin receptor substrate-1 may decrease insulin action

262 (8.4-fold, P < 0.01), paralleled by reduced insulin receptor substrate-1 mRNA expression (-0.7-fold,

263 sses forkhead box O3, B-cell lymphoma 2, and insulin receptor substrate 1 mRNAs in the cocultured SMC

264 DH) for knockout of the insulin receptor and insulin receptor substrate-1 on three genetic background

265 t defect in IR-stimulated phosphorylation of insulin receptor substrate-1 or activation of the phosph

266 n insulin-induced phosphorylation of the IR, insulin receptor substrate-1, or AKT, but it elicited ch

267 n turn affects serine 612 phosphorylation of insulin receptor substrate-1 (p612 IRS-1).

268 insulin signaling cascade (insulin receptor, insulin receptor substrate-1, p85, phosphatidylinositol

269 phorylation of type I IGF receptor (IGF-IR), insulin receptor substrate 1, phosphatidylinositol 3-kin

270 Expression of insulin receptor substrate 1, phosphatidylinositol 3-kin

271 receptor (IGF-1R) and formation of an IGF-1R/insulin receptor substrate-1/ phosphatidylinositol 3-kin

272 d expression of the key downstream messenger insulin receptor substrate-1 phosphorylated at serine re

273 vity and reduced glucocorticoid induction of insulin receptor substrate 1 phosphorylation at serine 3

274 pressor of cytokine signaling 3 (SOCS3), and insulin receptor substrate 1 phosphorylation.

275 ly a modest decrease in Stat6 activation and insulin receptor substrate-1 phosphorylation after IL-4

276 mRNA of the DUSP-5 and 2) increases hepatic insulin receptor substrate-1 phosphorylation at serine 6

277 rylation in muscle may explain the increased insulin receptor substrate 1, PI3K, and ERK phosphorylat

278 n a decrease of both fatty acid synthase and insulin receptor substrate-1 protein expression yet did

279 The level of insulin receptor substrate-1 protein was increased 2-fol

280 h factor receptor adaptor molecules, such as insulin receptor substrate-1, rather than the receptors

281 s to stimulate YXXM phosphorylation of IRS1 (insulin receptor substrate 1) required for PI3K/AKT acti

282 of HNF-4A gene (rs2144908 and rs1884614) and insulin receptor substrate 1 (rs1801278) are significant

283 We also found increased insulin receptor substrate-1 Ser(636) phosphorylation in

284 the level of the insulin receptor, increased insulin receptor substrate 1 (Ser-312), and decreased Ak

285 mpanied by consistent differences in hepatic insulin receptor substrate 1 serine phosphorylation and

286 duced Jun NH2-terminal kinase activation and insulin receptor substrate 1 serine phosphorylation in v

287 s also slightly decreased and the binding to insulin receptor substrate-1 slightly increased in brown

288 stabilization of a second messenger protein, insulin receptor substrate 1, that mediates PI 3-kinase-

289 fADN decreased phosphorylation of insulin receptor substrate-1 (Tyr-608), Akt (Thr-308 and

290 inase activity by 183 +/- 6% (p = 0.003) and insulin receptor substrate 1 tyrosine phosphorylation by

291 irmed with the absence of insulin-stimulated insulin receptor substrate 1 tyrosine phosphorylation.

292 s reduced, whereas serine phosphorylation of insulin receptor substrate 1 was elevated.

293 Downstream of IGF-IR, insulin receptor substrate 1 was phosphorylated, leading

294 ith these changes, serine phosphorylation of insulin receptor substrate 1 was reduced, and Akt activa

295 that of pyruvate dehydrogenase kinase 4 and insulin receptor substrate 1 was reduced.

296 racellular signal-regulated kinase, AKT, and insulin receptor substrate 1 was unaffected by ICI treat

297 scle expression of insulin receptor beta and insulin receptor substrate 1 were down-regulated 2-fold

298 on of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sen

299 d that insulin stimulated the association of insulin receptor substrate-1 with the p85alpha subunit o

300 IGF-I receptor from tyrosine phosphorylating insulin receptor substrate-1 without affecting tyrosine