ライフサイエンスコーパス: insulin receptor

1 e is insulin, which acts locally through the insulin receptor.

2 ion of a known synapse-promoting factor, the insulin receptor.

3 es the ubiquitination and degradation of the insulin receptor.

4 but also the cellular context of the mutant insulin receptor.

5 gs, but showed only very weak binding to the insulin receptor.

6 ermediate was fully active in binding to the insulin receptor.

7 n of either protein kinase B (Akt) or of the insulin receptor.

8 tes IRS1/2 and inhibits its binding with the insulin receptor.

9 in the liver upon its phosphorylation by the insulin receptor.

10 first leucine-rich repeat domain (L1) of the insulin receptor.

11 external insulin on local microcircuits via insulin receptors.

12 he result of lipotoxicity-associated loss of insulin receptors.

13 by 4-fold), (iii) enhances affinity for the insulin receptor (1.5 +/- 0.1-fold), and (iv) preserves

14 ts, high fat-fed insulin-resistant rats, and insulin receptor 2'-O-methoxyethyl chimeric antisense ol

15 eptor, a G-protein-coupled receptor, and the insulin receptor, a receptor tyrosine kinase.

16 that in ZDF rats, treatment with a synthetic insulin-receptor-activating peptide or with insulin to l

17 bition-mediated hepatocyte division involved insulin receptor activation and was mediated by the mech

18 in the developing Xenopus visual system, and insulin receptor activation increases dendritic spine de

19 the principal signaling module downstream of insulin receptor activation that regulates the accumulat

20 Of note, insulin receptor activation was not required for glucose

21 ese rats, which was associated with improved insulin receptor activation.

22 sociated with alterations in Let-7 levels or insulin receptor activation.

23 , mediate the phosphorylation of PREX2 after insulin receptor activation.

24 sport contributes to regulation of endosomal insulin receptor activity and glucose homeostasis in hep

25 enzyme and cathepsin D were impaired; hence insulin receptor activity increased.

26 in receptor substrate-2 (Irs2), an essential insulin receptor adaptor protein.

27 days of treatment with either insulin or the insulin receptor agonist peptide S597.

28 Hyperglycemia induced by treatment with the insulin receptor agonist S961 increased Deaf1-Var1 and P

29 ike growth factor 2 and the A-isoform of the insulin receptor, allowing aberrant activation of mitoge

30 namely the helical C-terminal segment of the insulin receptor alpha-chain (termed alphaCT).

31 We have recently uncovered an insulin receptor and adrenergic receptor signal network

32 Both insulin receptor and Akt phosphorylation were abrogated

33 n mice heterozygous for a null allele of the insulin receptor and an N-ethyl-N-nitrosourea-induced al

34 BRD4 from chromatin at regulatory regions of insulin receptor and EGFR family RTKs to reduce their ex

35 In primary neurons, apoE4 interacts with insulin receptor and impairs its trafficking by trapping

36 otein), an adaptor protein that binds to the insulin receptor and inhibits insulin signaling, increas

37 Insulin receptor and insulin-like growth factor type I r

38 ulin's delivery to the brain mediated by the insulin receptor and is it a regulated process?

39 e found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxralpha produced equi

40 In normal muscle plakoglobin binds the insulin receptor and PI3K subunit p85 and promotes PI3K-

41 Compounds that can enhance insulin receptor and post-receptor signalling cascades o

42 CHO cells overexpressing the human insulin receptor and rat IRS1 were stimulated with insul

43 ice with hepatocyte-specific deletion of the insulin receptor and their controls.

44 or small molecule agents directed toward the insulin receptor and/or the type 1 insulin-like growth f

45 Nonetheless, insulin receptors and insulin-responsive glucose transpo

46 iescent tumour endothelial cells with intact insulin receptors and partly prevented increases in VCAM

47 factor receptors (i.e., EGF-receptor but not insulin receptor) and pathogen recognition receptors (PR

48 es IRS1/2, inhibits its association with the insulin receptor, and disrupts insulin signaling.

49 that regulatory T cells (Tregs) express the insulin receptor, and that high levels of insulin impair

50 Insulin receptor antagonism increased pancreatic beta-ce

51 We used the insulin receptor antagonist S961 to induce severe insuli

52 Here we use administration of the insulin receptor antagonist S961, shown to increase beta

53 h-fat diet or from the administration of the insulin receptor antagonist S961.

54 D challenge or short term treatment with the insulin receptor antagonist S961.

55 ic db/db mice and in WT mice treated with an insulin receptor antagonist, revealing metabolic control

56 ectively in regions of the hippocampus where insulin receptors are expressed, and occludes the neuron

57 owed that ApoE3 had greater association with insulin receptor as compared to ApoE4, regardless of Abe

58 tory protein Munc18c, a direct target of the insulin receptor, as a molecular switch to coordinate th

59 Insulin receptors, as well as IGF-1 receptors and their

60 Moreover, insulin receptor autophosphorylation is dependent on int

61 d normal chow, skeletal muscle expression of insulin receptor beta and insulin receptor substrate 1 w

62 Finally, by deleting insulin receptor beta in the Myf5 lineage, we provide in

63 SAHA decreased phosphorylation of insulin receptor beta, Akt, and the Akt substrate FoxO1,

64 -fold reduction in renal cortical homogenate insulin receptor-beta among knockout mice compared with

65 tion returning to normal, causing persistent insulin receptor-beta inhibition.

66 these mice indeed became hyperglycemic after insulin receptor blockade.

67 ted by insulin signaling and reversed by the insulin receptor blocker AGL2263.

68 inding protein 14 (Grb14) is an inhibitor of insulin receptor catalytic activity, highly expressed in

69 Insulin receptors co-immunoprecipitate MHCI from hippoca

70 nt first structural insight into the insulin-insulin receptor complex, the role of the C terminus of

71 Dominant-negative insulin receptor constructs decrease synapse density in

72 Because LK neurons express the insulin receptor (dInR), we tested functional links betw

73 of synthetic peptides that interact with the insulin receptor ectodomain have been discovered by phag

74 ulates MBNL1-mediated splicing activation of insulin receptor exon 11 and found that MBNL1 activates

75 e such event is MBNL1-mediated activation of insulin receptor exon 11 inclusion, which requires an in

76 ides new information about the importance of insulin receptors expressed in collecting duct principal

77 They activate glycogen synthase in insulin receptor-expressing CHO-IR cells and primary rat

78 hy created by a fat-specific knockout of the insulin receptor (F-IRKO) or both IR and insulin-like gr

79 ing receptor dimer--resembling signalling by insulin receptor family members, which share similar ext

80 Studies in the insulin receptor FOXO1 KO mouse indicate that insulin is

81 Here, we selectively knocked out the insulin receptor from the proximal tubules of mice.

82 infused IRKO mice, with targeted deletion of insulin receptor from tubule epithelial cells of the kid

83 less/Wnt pathway activity, which upregulated insulin receptor gene expression to promote insulin sens

84 -1 (IRS1) feedback and reduced abundances of insulin receptor, GLUT4, AS160, ribosomal protein S6, an

85 studies of insulin bound to fragments of the insulin receptor have recently defined the topography of

86 ll (EC)-specific overexpression of the human insulin receptor (hIRECO) using the Tie2 promoter-enhanc

87 target genes include SOCS3, an inhibitor of insulin receptor, holo-RBP suppresses insulin responses

88 While Abeta can bind to insulin receptor, how ApoE isoforms modulate this intera

89 ced ternary complex formation with the IGF1R/insulin receptor hybrid.

90 (KOs) in mice of leptin receptor (L(2.1)KO), insulin receptor (I(2.1)KO), and double KOs of both rece

91 ctively competed with (125)I-insulin for the insulin receptor (IC50 = 10.6 nM) comparable to that for

92 ge in diabetes: (i) reduced concentration of insulin receptor, (ii) reduced concentration of insulin-

93 Mice lacking the insulin receptor in AgRP neurons (AgRP IR KO) exhibited

94 Here, we show that signaling from the insulin receptor in Drosophila neurons determines flies'

95 oblast-specific overexpression of or loss of insulin receptor in HFD-fed mice.

96 In mice that lack the insulin receptor in the brain, hepatic TG secretion was

97 ough it is known that insulin also activates insulin receptor in the dorsal vagal complex (DVC) to lo

98 tabolic features similar to mice lacking the insulin receptor in the osteoblast, including peripheral

99 n together, these results support a role for insulin receptor in the proximal tubule in the modulatio

100 Knockout of insulin receptors in endothelial cells also increased le

101 Surprisingly, targeted deletion of insulin receptors in intestinal epithelial cells in Apc(

102 Here we show that two insulin receptors in the migratory brown planthopper Nil

103 d, we generated Apc(Min/+) mice with loss of insulin receptors in vascular endothelial cells.

104 specific expression of CCR5, associated with insulin receptors, in the hypothalamic arcuate nucleus (

105 Thus, insulin receptor inactivation in ECs does not impair ins

106 Further studies of IGF-1R and insulin receptor inhibitors, together with genetic profi

107 o regulate the transcriptional activation of insulin receptor (InR) and adipose lipase brummer (bmm).

108 70 S6 kinase (S6k), acting downstream of the insulin receptor (InR) and the small GTPase Arf6, is a k

109 Expression of the insulin receptor (InR) gene itself appears to play an im

110 It was previously shown that Insulin receptor (InR) pathway signaling is essential fo

111 When expression of the sole Drosophila insulin receptor (InR) was reduced in larval fat bodies,

112 s as key markers predisposing to depression (insulin receptors Insr, glucose transporters Glut-4 and

113 tion, we generated knockout mice lacking the insulin receptor (InsR KO) specifically in the collectin

114 adigm for insulin signaling centers upon the insulin receptor (InsR) and its substrate IRS1; the latt

115 A custom TaqMan array identified increased insulin receptor (INSR) gene expression; immunoblot anal

116 Loss of function of the insulin receptor (INSR) in humans produces severe insuli

117 ve previously shown that the closely related insulin receptor (InsR) is expressed in tamoxifen-resist

118 PKCepsilon) and the consequent inhibition of insulin receptor (INSR) kinase activity.

119 Women with insulin receptor (INSR) mutations develop severe hyperan

120 Because defective placental insulin receptor (InsR) signaling is a hallmark of pregn

121 etes (T2D) and is characterized by defective insulin receptor (INSR) signalling.

122 not observed in multiple RNAs including the Insulin Receptor (Insr), Cardiac Troponin T (Tnnt2), Lim

123 dent dioxygenase (FTO), interleukin 6 (IL6), insulin receptor (INSR), neuronal growth regulator 1 (NE

124 ng status of six of the genes, including the insulin receptor (INSR), which may play a role in growth

125 ption and accompanied by upregulation of the insulin receptor (INSR).

126 epidermal growth factor receptor (EGFR) and insulin receptor (InsR)/insulin-like growth factor recep

127 factor 1 (IGF1), IGF1 receptor (IGF1R), and insulin receptor (INSR); whereas in mammals, positively

128 Insulin activates insulin receptors (InsRs) in the hypothalamus to signal

129 components in the insulin-signaling pathway (insulin receptor, insulin receptor substrate-1, and Akt)

130 al situation; and that in beta-cells lacking insulin receptors, insulin and glucose minimally activat

131 We show that the insulin receptor (IR) and downstream signals can be acti

132 Despite a high degree of homology, insulin receptor (IR) and IGF-1 receptor (IGF1R) mediate

133 Insulin binds to the insulin receptor (IR) and induces tyrosine phosphorylati

134 we found that Gal3 can bind directly to the insulin receptor (IR) and inhibit downstream IR signalin

135 proliferation, migration, and activation of insulin receptor (IR) and insulin growth factor-1 recept

136 The insulin receptor (IR) and insulin-like growth factor-1 r

137 resulted in an up-regulated signaling of the insulin receptor (IR) and its downstream signaling molec

138 e insulin analogs with affinity for both the insulin receptor (IR) and mannose receptor C-type 1 (MR)

139 ed for predicting both the activation of the insulin receptor (IR) and the redistribution of glucose

140 n-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR) are promising therapeutic agents i

141 4548-G05 selectively activates an insulin receptor (IR) but not insulin-like growth factor

142 Because the insulin receptor (IR) can traffic to the nucleus, and Ca

143 Here, we show that disruption of insulin receptor (IR) expression in beta cells has a dir

144 We disrupted the insulin receptor (IR) gene specifically in the theca-int

145 shes the plasma membrane localization of the insulin receptor (IR) in hepatocytes.

146 Because of the defect on insulin receptor (IR) in the trophoblast of the gestatio

147 MBH insulin receptor (IR) levels and signaling are increased

148 Gaining the full activity of the insulin receptor (IR) requires the proteolytic cleavage

149 A hallmark of type 2 diabetes is impaired insulin receptor (IR) signaling that results in dysregul

150 Defective hepatic insulin receptor (IR) signalling is a pathogenic manifes

151 that SORLA acts as a sorting factor for the insulin receptor (IR) that redirects internalized recept

152 imer in the crystal structure of the related Insulin Receptor (IR) with Insulin bound that allows dir

153 hibited insulin-dependent phosphorylation of insulin receptor (IR), AKT, and extracellular signal-rel

154 ulin-like growth factor 1 receptor (IGF-IR), insulin receptor (IR), and other oncoproteins.

155 egulatory element-binding protein (SREBP-1), insulin receptor (IR), and PPARgamma in liver were measu

156 adipose tissue, we created mice lacking the insulin receptor (IR), IGF-1 receptor (IGF1R), or both u

157 (M2), IGF-I, and NPH insulin to activate the insulin receptor (IR)-A and IR-B and IGF-I receptor (IGF

158 sociations are stronger in tumors expressing insulin receptor (IR).

159 or (IGF-1R) and its close family member, the insulin receptor (IR).

160 Endogenous hyperinsulinemia and insulin receptor (IR)/IGF-I receptor (IGF-IR) phosphoryl

161 ty to the IGF-1R and to the A isoform of the insulin receptor (IR-A) failed to promote NSC growth.

162 rentially bind to the metabolic B-isoform of insulin receptor (IR-B).

163 cells from individuals with mutations in the insulin receptor (IR-Mut) into functional myotubes and c

164 n-stimulated GU, proximal insulin signaling (insulin receptor [IR] tyrosine phosphorylation, IR subst

165 kinase pathway, recent studies indicate that insulin receptors (IRs) and insulin-like growth factor 1

166 Insulin receptors (IRs) are expressed in discrete neuron

167 Domain-minimized insulin receptors (IRs) have enabled crystallographic an

168 Postnatal ablation of insulin receptors (IRs) in glial fibrillary acidic prote

169 Insulin receptors (IRs) on endothelial cells may have a

170 Because insulin acting through the insulin receptor is a survival factor for many cancer ce

171 ineage, we provide in vivo evidence that the insulin receptor is essential for adipogenesis and that

172 Insulin receptor is recruited to the cilium of stimulate

173 with different affinities to closely related insulin receptor isoforms A and B (IR-A and IR-B) and in

174 The catalytic and allosteric mechanisms of insulin receptor kinase (IRK) are investigated by a comb

175 Insulin binding changes conformation of the insulin receptor kinase (IRK) domain and initiates gluco

176 in to bilirubin and is directly activated by insulin receptor kinase (IRK).

177 on, for studies in either beta-cell specific insulin receptor knock-out (betaIRKO) or control mice.

178 To determine how insulin receptor knockdown enhances SS1P action, we anal

179 ts in the liver, we generated liver-specific insulin receptor knockout (LIRKO) and IR/FoxO1 double kn

180 er, tamoxifen-induced cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post

181 Liver-specific ablation of the IR (L-Insulin Receptor KO) induces glucose intolerance, insuli

182 YXWF motif of S519C16 are seen to engage the insulin receptor L1 domain surface in a fashion almost i

183 cancer cell lines, we explored how lowering insulin receptor level would affect the cytotoxic action

184 ng mice with muscle-specific deletion of the insulin receptor (M-IR-/- mice), the IGF-1 receptor (M-I

185 which IRS2, MTOR, and cyclin D2, but not the insulin receptor, mediate glucose-induced proliferation.

186 ic insulin signaling revealed an increase in insulin receptor-mediated Akt phosphorylation in hCOX-2

187 Conversely, enhanced insulin receptor-mediated signaling and reduced levels o

188 B8)]proinsulin protein molecule bound to the insulin receptor more effectively than wild-type proinsu

189 Characterization of overt hyperglycemia in insulin receptor mutant (Insr(P1195L/+)) mice exposed to

190 ent stem cells (iPSCs) from individuals with insulin receptor mutations and age-appropriate control s

191 ients with genetic insulin resistance due to insulin receptor mutations.

192 These findings indicate that the insulin receptor negatively regulates immunotoxin action

193 t mice with a brain-specific knockout of the insulin receptor (NIRKO mice) exhibit brain mitochondria

194 Our studies showed that insulin receptors on the endothelium are important for i

195 sulin signaling disrupted by ablation of the insulin receptor or Akt.

196 nsulin signalling by genetic ablation of the insulin receptor or the regulatory subunits phosphatidyl

197 Thus, signalling via the insulin receptor, p85, and XBP1 maintains podocyte homeo

198 es signals from multiple receptors including insulin receptors, pathogen-associated molecular pattern

199 isplayed increased pancreatic mRNA levels of insulin receptors, Pdx1 and Igf1R, suggesting adiponecti

200 Neither insulin receptor phosphorylation nor the interaction bet

201 h was also observed in murine models bearing insulin receptor positive tumors.

202 ite adipose tissue has been shown to inhibit insulin receptor responses.

203 Inactivating mutations in the insulin receptor results in extreme insulin resistance.

204 Moreover, altered insulin receptor signaling and insulin resistance can mo

205 animals rescues synapse density, identifying insulin receptor signaling as a critical mediator of the

206 ted that insulin resistance is caused by low insulin receptor signaling attributable to its abnormal

207 Thus, reduced insulin receptor signaling in IMCD could contribute to h

208 Pharmacologically inhibiting insulin receptor signaling in MHCI-deficient animals res

209 sults identify an important role for an MHCI-insulin receptor signaling pathway in circuit patterning

210 taxane resistance through activation of IGF1/insulin receptor signaling.

211 e neuronal insulin response by de-repressing insulin receptor signaling.

212 paired clearance of insulin, which amplified insulin receptor signaling.

213 ent of cells with a PI 3-kinase inhibitor or insulin receptor silencing with RNA interference abolish

214 residue within the B24-binding pocket of the insulin receptor; similar molecular principles are likel

215 Insulin receptor substrate (IRS) 2 as intermediate docki

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

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

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

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

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

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

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

223 13 bind IL-4 receptors, which signal through insulin receptor substrate (IRS)-2, inducing M2 macropha

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

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

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

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

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

229 -1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdow

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 Insulin receptor substrate 1 (IRS1) was overexpressed in

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

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

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

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

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

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

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

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

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

255 3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, there

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

257 Insulin receptor substrate 2 (IRS2) suppression induced

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 nd MHCI unmasks a cytoplasmic epitope of the insulin receptor that mediates downstream signaling.

287 ingolipid acyl chain length directly affects insulin receptor translocation and subsequent signaling.

288 IRS1 and IRS2 are key substrates of the insulin receptor tyrosine kinase.

289 Epidermal growth factor (EGF) and insulin receptor tyrosine kinases (RTKs) exemplify how r

290 1 modulates the activity of PTP1B, the major insulin receptor tyrosine phosphatase.

291 Furthermore, LTB4 decreased insulin receptor tyrosine phosphorylation in hepatocytes

292 of free saturated fatty acids, which promote insulin receptor ubiquitination and subsequent degradati

293 io of the IGF-II-sensitive, A isoform of the insulin receptor versus the IR-B isoform, which when sti

294 The insulin receptor was detected on both neurons and glia,

295 cade in vivo in physiological states via the insulin receptor, we designed two experimental approache

296 ILPs function by binding to the insulin receptor, which activates downstream components

297 5, belongs to a clade of RTKs related to the insulin receptor, which are distinguished by an extracel

298 ll molecule inhibitor of both IGF-1R and the insulin receptor, which has shown acceptable tolerabilit

299 L-DKP ester insulin bound weakly to the insulin receptor, while synthetic L-DKP insulin derived

300 -Site 1 fusion peptide, S519, that binds the insulin receptor with subnanomolar affinity and exhibits