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

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

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

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

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

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

27 roximal signaling molecules (IRTK as well as insulin receptor substrate 1 and phosphatidylinositol 3-

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

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

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

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

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

33 Insulin receptor substrate-1 and -2 phosphorylation and

34 ciated with defects in insulin activation of insulin receptor substrate-1 and -2-associated phosphati

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

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

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

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

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

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

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

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

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

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

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

46 Insulin-induced tyrosine phosphorylation of insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 cooperatively to effectively increase local insulin receptor substrate 1 concentration at the membra

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

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

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

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

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

86 In the absence of insulin receptor substrate-1, functional impairment of a

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 R-beta), +/+ 34%, db/+ 57% decrease, P<0.05; insulin receptor substrate 1 (IRS-1), +/+ 44%, db/+ 61%

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

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

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

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

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

124 -1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdow

125 ine phosphorylation of the insulin receptor, insulin receptor substrate 1 (IRS-1), and IRS-2 was redu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 frequencies of the Gly972Arg variant of the insulin receptor substrate-1 (IRS-1) gene and the Ala54T

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

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

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

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

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

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

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

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

163 Insulin receptor substrate-1 (IRS-1) is pivotal in media

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 ed a phosphoprotein of 170 kDa identified as insulin receptor substrate-1 (IRS-1), whereas INR betaDe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 Insulin receptor substrate 1 (IRS1) was overexpressed in

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

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

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

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

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

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

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

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

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

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

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

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

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

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 horylation of insulin receptor beta-subunit, insulin receptor substrate-1, or Akt but stimulated the

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

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

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

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

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

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

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

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

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

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

287 lution of an amino-terminal segment of human insulin receptor substrate 1 that encompasses its plecks

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