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

1 sozyme (RCAM-lysozyme), a well characterized insulin receptor substrate.

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

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

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

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

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

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

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

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

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

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

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

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

14 -1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdow

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 Insulin receptor substrate 1 (IRS1) was overexpressed in

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

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

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

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

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

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

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

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

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

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

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

54 884614, OR=2.44, CI=1.42-4.48, P=0.002), and insulin receptor substrate 1 AA+AG (rs1801278, OR=2.71,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 stance through inhibitory phosphorylation of insulin receptor substrate 1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 2 interacts with and directly phosphorylates insulin receptor substrate-1 in cardiomyocytes, causing

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

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

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

159 (8.4-fold, P < 0.01), paralleled by reduced insulin receptor substrate-1 mRNA expression (-0.7-fold,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 cking either insulin receptors (betaIRKO) or insulin receptor substrate 2 (betaIRS2KO).

179 Appropriate regulation of insulin receptor substrate 2 (IRS-2) expression in pancr

180 Insulin receptor substrate 2 (IRS-2) plays a critical ro

181 ubsequent 52% decrease in insulin-stimulated insulin receptor substrate 2 (IRS-2) tyrosine phosphoryl

182 cAMP response element-binding protein (CREB)-insulin receptor substrate 2 (Irs-2), and increased beta

183 the brain, targets insulin receptor (INSR), insulin receptor substrate 2 (IRS-2), and insulin-degrad

184 that promotes beta-cell growth and survival, insulin receptor substrate 2 (IRS-2), is a member of a f

185 insulin-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2), whereas it had min

186 teins involved in insulin signaling, such as insulin receptor substrate 2 (IRS2) and glucose transpor

187 3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, there

188 component of all types of diabetes, and the insulin receptor substrate 2 (IRS2) branch of signaling

189 a/cAMP mediates these actions by stimulating insulin receptor substrate 2 (IRS2) expression.

190 s, proliferation, and survival by increasing insulin receptor substrate 2 (IRS2) levels and identify

191 Insulin receptor substrate 2 (IRS2) suppression induced

192 s is sufficient to enhance the expression of insulin receptor substrate 2 (IRS2) to levels observed i

193 2)-associated binding proteins 1-3 (GAB1-3), insulin receptor substrate 2 (IRS2), docking protein 1 (

194 mice lacking insulin signaling intermediate insulin receptor substrate 2 (IRS2), we confirmed that h

195 The study also provides strong evidence that insulin receptor substrate 2 (Irs2), which is known to h

196 ronic morphine-induced downregulation of the insulin receptor substrate 2 (IRS2)-thymoma viral proto-

197 s (week 15); liver and adipose AhR and IRS2 (insulin receptor substrate 2) mRNA abundance, and PCB-77

198 Moreover, miR-33a and -b also target the insulin receptor substrate 2, an essential component of

199 results in enhanced IR signaling through the insulin receptor substrate 2-AKT pathway in beta-cells a

200 Insulin receptor substrate-2 (IRS-2) belongs to the IRS

201 related with tyrosine phosphorylation of the insulin receptor substrate-2 (IRS-2) in macrophages.

202 Insulin receptor substrate-2 (IRS-2) plays a critical ro

203 Insulin receptor substrate-2 (IRS-2) plays an essential

204 to abused drugs decreases the expression of insulin receptor substrate-2 (IRS-2; a protein involved

205 of sarcomas and found a marked induction of insulin receptor substrate-2 (IRS2) and phosphorylated A

206 hat mice heterozygous for a null mutation in insulin receptor substrate-2 (Irs2) display a 17% increa

207 3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstr

208 Insulin receptor substrate-2 (Irs2) is a critical mediat

209 Here, we show that, in mice, less insulin receptor substrate-2 (Irs2) signaling throughout

210 We identify insulin receptor substrate-2 (Irs2), a known cAMP-respon

211 ing through direct and indirect induction of insulin receptor substrate-2 (Irs2), an essential insuli

212 In a separate cohort, phosphorylated insulin receptor substrate-2 (pIRS-2) and insulin growth

213 ysis occurs normally in B cells deficient in insulin receptor substrate-2 or the p85alpha subunit of

214 The hepatic mRNA level of the HIF-2 target insulin receptor substrate-2 was higher, whereas that of

215 lts in decreased tyrosine phosphorylation of insulin receptor substrate-2 with impeded insulin signal

216 n key insulin-signaling molecules, including insulin receptor substrate-2, and substrate metabolism t

217 ic screen of HD, we found that activation of insulin receptor substrate-2, which mediates the signali

218 ximately 40% reduction in insulin-stimulated insulin receptor substrate-2-associated phosphatidylinos

219 Using mass spectrometric analysis insulin receptor substrate 4 (IRS-4) has been identified

220 One interacting protein was insulin receptor substrate 4 (IRS-4), a member of the IR

221 ation of PVH and peri-PVH neurons expressing insulin-receptor substrate 4 (IRS4(PVH)) involved in ene

222 hyperinsulinemic-euglycemic clamp and muscle insulin receptor substrate and Akt phosphorylation demon

223 thways governing glucose metabolism, such as insulin receptor substrate and Akt substrate.

224 PKR also directly targets and modifies insulin receptor substrate and hence integrates nutrient

225 ased brain glucose uptake, activation of the insulin receptor substrate and of the PI3K/Akt signaling

226 phosphorylation nor the interaction between insulin receptor substrate and phosphatidylinositide 3-k

227 TNF-alpha inhibits the function of insulin receptor substrates and decreases the expression

228 teosomal degradation of the docking protein, insulin receptor substrate, and enhanced signaling throu

229 ugh serine phosphorylation and inhibition of insulin receptor substrate by the downstream effector of

230 n the level of serine phosphorylation of the insulin receptor substrate IRS-1.

231 These foci contain the insulin receptor substrate (IRS) 1 adaptor molecule, and

232 easured the life span of mice lacking either insulin receptor substrate (IRS) 1 or 2, the major intra

233 Insulin receptor substrate (IRS) 2 as intermediate docki

234 IS/TOR network, including the critical nodes insulin receptor substrate (IRS) and phosphatidylinosito

235 The insulin receptor substrate (IRS) proteins are cytoplasmi

236 The insulin receptor substrate (IRS) proteins are cytoplasmi

237 ammatory cytokines induce phosphorylation of insulin receptor substrate (IRS) proteins at Ser sites t

238 The insulin receptor substrate (IRS) proteins represent a cr

239 The insulin receptor substrate (IRS) proteins serve as essen

240 naling and the extent to which alteration of insulin receptor substrate (IRS) signaling modulates bet

241 The mRNA transcript levels of AAH, insulin receptor substrate (IRS), insulin and insulin-li

242 CS)3 deficiency increases insulin-stimulated insulin receptor substrate (IRS)-1 and -2 phosphorylatio

243 ficiency suppressed the up-regulation of the insulin receptor substrate (IRS)-1 and IRS-2 and thereby

244 Hepatic insulin receptor substrate (IRS)-1 and IRS-2 expression

245 l line decreased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2 in response

246 o delayed and impaired activation of hepatic insulin receptor substrate (IRS)-1 and IRS-2 signaling,

247 xpression of major IGF signaling components, insulin receptor substrate (IRS)-1 and IRS-2, an effect

248 of mRNAs for insulin receptor (IR)A and IRB; insulin receptor substrate (IRS)-1 and IRS-2; phosphoino

249 g SOCS3 and via SOCS3-mediated inhibition of insulin receptor substrate (IRS)-1 and possibly AMPK in

250 Suppression of insulin receptor substrate (IRS)-1 and tuberous sclerosi

251 Research has focused on insulin receptor substrate (IRS)-1 as a locus for insuli

252 association between genetic variants of the insulin receptor substrate (IRS)-1 gene, platelet functi

253 xamine the role of serine phosphorylation of insulin receptor substrate (IRS)-1 in mediating fat-indu

254 Ad-GLP-1 treatment increased basal levels of insulin receptor substrate (IRS)-1 in the liver and acti

255 in (10(-8) to 10(-7) m) for 0-24 h increased insulin receptor substrate (IRS)-1 phosphorylation at Se

256 yotubes, dexamethasone (> or = 24 h) reduced insulin receptor substrate (IRS)-1 protein and PI3K/Akt

257 tein kinase (PKC)theta activation, increased insulin receptor substrate (IRS)-1 serine 1101 phosphory

258 Insulin receptor and insulin receptor substrate (IRS)-1 serine hyperphosphory

259 rough inactivation of S6K1, stabilization of insulin receptor substrate (IRS)-1, and increased signal

260 increased insulin receptor signaling, i.e., insulin receptor substrate (IRS)-1, insulin receptor pho

261 raised insulin-like growth factor-1 (IGF-1), insulin receptor substrate (IRS)-1, vascular endothelial

262 is, p85alpha mRNA and protein expression and insulin receptor substrate (IRS)-1-associated PI 3-kinas

263 Phosphorylation of insulin receptor substrate (IRS)-1/2 by IGF-I receptor t

264 betes reduced basal insulin receptor kinase, insulin receptor substrate (IRS)-1/2-associated phosphat

265 sulin-like growth factor receptor-1 (IGF-1R)/insulin receptor substrate (IRS)-1/Akt pathway with ERal

266 the insulin receptor catalytic activity and insulin receptor substrate (IRS)-1/IRS-2 dephosphorylati

267 educed strength of insulin signaling via the insulin receptor substrate (IRS)-1/phosphatidylinositol

268 -restricted phosphopeptides derived from the insulin receptor substrate (IRS)-2 and the cell-cycle re

269 bited insulin-induced Tyr phosphorylation of insulin receptor substrate (IRS)-2 protein and the activ

270 Furthermore, we also showed that insulin receptor substrate (IRS)-2, but not IRS-1, is in

271 13 bind IL-4 receptors, which signal through insulin receptor substrate (IRS)-2, inducing M2 macropha

272 stimulating downstream proteins through the insulin receptor substrate (IRS).

273 Postreceptor signaling through the insulin receptor substrate (IRS)/PI3-K/Akt pathway was e

274 ikely caused by, direct dephosphorylation of insulin receptor substrate (IRS)1/2 in the liver, accomp

275 We found insulin receptor substrate (IRS)2 and enhanced-activated

276 Pituitaries responded to insulin through insulin receptor substrate (IRS)2 but not IRS1, whereas

277 ort an altered interrelationship between the insulin receptor substrate (IRS-1) and Akt/mTOR pathway

278 ociation with more phospho (P)-serine-type 1 insulin receptor substrate (IRS-1) and less P-tyrosine-I

279 When phosphorylated by mTORC1/S6K, the insulin receptor substrate (IRS-1) is targeted for ubiqu

280 ceptors (IR) resulting in phosphorylation of insulin receptor substrates (IRS) inducing activation of

281 e effects are mediated, at least in part, by insulin receptor substrates (IRS), one of which is insul

282 Insulin receptor substrates (Irs-proteins) integrate sig

283 ut displayed severely blunted signalling via insulin-receptor substrate (IRS) proteins, key mediators

284 d phosphorylation of IGF signaling molecules insulin-receptor substrate (IRS)-1 and IRS-2.

285 ne kinase (MCK)-Cre to disrupt expression of insulin receptor substrates Irs1 and Irs2 in mouse skele

286 resistin increased serine phosphorylation of insulin receptor substrate (IRS1) through the activation

287 tyrosine phosphorylation of adapter protein insulin receptor substrate (IRS1).

288 Insulin receptor substrates (IRSs) are signaling adaptor

289 gnaling for energy uptake and growth through insulin receptor substrates (IRSs), which interact with

290 ovel PDZ1 binding partner, the I-BAR protein insulin receptor substrate p53 (IRSp53).

291 improved insulin signal transduction via the insulin receptor substrate-phosphatidylinositol-3-hydrox

292 hese hormones induces cell signaling via the insulin receptor substrate/phosphatidylinositol 3-kinase

293 pathways in rodent beta-cells, including the insulin receptor substrate/phosphatidylinositol-3 kinase

294 ing selectively in endothelial cells via the insulin receptor substrate/PI3K/Akt pathway to reduce th

295 The 53 kDa insulin receptor substrate protein (IRSp53) is highly en

296 ess at least two Tiam1-interacting proteins, insulin receptor substrate protein 53 kDa (IRSp53) and s

297 of the insulin signaling pathways engaged by insulin receptor substrate proteins.

298 ting Tyr-325 was not required for the robust insulin receptor substrate response.

299 results from differential downregulation of insulin receptor substrates that control phosphatidylino

300 sed muscle insulin signaling (phosphorylated insulin receptor substrate(Tyr) and Akt(Ser473) levels)