ライフサイエンスコーパス: insulin receptor

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

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

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

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

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

6 depleting the cell surface population of the insulin receptor.

7 ource of minimized ligands of the vertebrate insulin receptor.

8 nces, yet all bind to and activate the human insulin receptor.

9 increased levels of an activated form of the insulin receptor.

10 sulin resistance, presumably through defunct insulin receptors.

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

12 mechanism controlled by the autocrine IGF-II-insulin receptor-A specific signaling axis.

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

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

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

16 g of the glucose transporter GLUT4 driven by insulin receptor activation provides the prototypic exam

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

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

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

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

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

22 strong albumin binding, and by lowering the insulin receptor affinity 500-fold to slow down receptor

23 profile was also a significant reduction of insulin receptor affinity.

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

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

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

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

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

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

30 through an adaptive response involving IGF1R/insulin receptor and co-targeting these pathways may pro

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

32 Expression of insulin receptor and epidermal growth factor receptor wa

33 Mice lacking both the insulin receptor and FoxO1 (LIRFKO) exhibit reduced beta

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

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

36 vation of JNK enhances the expression of the insulin receptor and initiates the insulin-Myc signaling

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

38 made in the past decade in understanding the insulin receptor and its signalling pathways in cancer,

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 iverse strategies to activate the vertebrate insulin receptor and provide unique insight into the des

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 Insulin receptor antagonism increased pancreatic beta-ce

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

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

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

53 Importantly, pretreatment with the insulin receptor antagonist, GSK1838705, significantly s

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

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

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

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

58 ug treatment co-targeting mTORC1/2 and IGF1R/insulin receptor attenuated pAkt T308 and showed synergi

59 Moreover, insulin receptor autophosphorylation is dependent on int

60 sulin-stimulated tyrosine phosphorylation of insulin receptor beta (IRbeta) in mice fed a low-fat die

61 in sensitivity was associated with increased insulin receptor beta and insulin receptor substrate 1 a

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

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

64 ophin, epidermal growth factor receptor, and insulin receptor-beta; decreased Ras homolog gene family

65 al cerebral blood flow within areas dense in insulin receptors (bilateral amygdala) in response to in

66 these mice indeed became hyperglycemic after insulin receptor blockade.

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

68 significantly higher binding affinity to the insulin receptor compared with the native insulin, resul

69 Dominant-negative insulin receptor constructs decrease synapse density in

70 acking IRs in astrocytes (astrocyte-specific insulin receptor deletion [IRKOGFAP] mice).

71 Blockade of arcuate nucleus insulin receptors did not lower SNA in pregnant or non-p

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 present the structure of the entire dimeric insulin receptor ectodomain saturated with four insulin

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

76 ociated with changes in arcuate NPY neuronal insulin receptor expression.

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

78 r (IRR) is a receptor tyrosine kinase of the insulin receptor family and functions as an extracellula

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

82 abolic parameters, cognitive function, brain insulin receptor function, synaptic plasticity, dendriti

83 ction mutations in both alleles of the human insulin receptor gene (INSR) cause extreme insulin resis

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

85 ADRbeta2, insulin receptor, glycogen content and citrate synthase

86 monoclonal antibody (MAb) against the human insulin receptor (HIR).

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

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

89 ough reduced tyrosine kinase activity of the insulin receptor; however, its impact on pancreatic beta

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

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

92 A truncated version of the only insulin receptor in C. elegans has been discovered.

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

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

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

96 Knockout of insulin receptors in endothelial cells also increased le

97 ty or rescue processing of newly synthesized insulin receptors in ER-stressed cells.

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

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

100 retion is lost following genetic ablation of insulin receptors in the somatostatin-secreting delta-ce

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

102 e transport genes (glucose transporter-2 and insulin receptor) in the jejunum.

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

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

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

106 70 S6 kinase (S6k), acting downstream of the insulin receptor (InR) and the small GTPase Arf6, is a k

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

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

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

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

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

112 Using a T reg-specific insulin receptor (Insr) deletion model, we found that di

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

114 nsulin-like growth factor 1 receptor (IGF1R)/insulin receptor (INSR) is critical for blocking prolife

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

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

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

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

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

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

121 , an abundant microRNA in the brain, targets insulin receptor (INSR), insulin receptor substrate 2 (I

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

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

124 mitophagy and mitochondrial accumulation of insulin receptor (INSR).

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

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

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

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

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

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

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

132 report the cryo-EM structure of full-length insulin receptor (IR) and insulin complex in the active

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

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

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

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

137 with spindle checkpoint proteins to promote insulin receptor (IR) endocytosis through recruiting the

138 ice with liver-specific knockout (KO) of the insulin receptor (IR) have a 50% reduction in Arrdc3 mes

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

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

141 eceptor knockout (SIRKO) mouse, in which the insulin receptor (IR) is inactivated only in skin, with

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

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

144 (LRP2)-dependent mechanism, coupled with the insulin receptor (IR) signaling cascade.

145 Insulin receptor (IR) signaling is central to normal met

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

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

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

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

150 vel, insulin exerts its function through the insulin receptor (IR), a transmembrane receptor tyrosine

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

152 novel, non-signaling isoform of the nematode insulin receptor (IR), DAF-2B, that modulates insulin si

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

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

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

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

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

158 his defect, we generated mice overexpressing insulin receptors (IR) specifically in skeletal muscle (

159 owth factors 1 and 2 (IGF-1 and -2) activate insulin receptors (IR-A and -B) and the IGF-1 receptor (

160 which we have specifically inactivated both insulin receptors (IRs) and IGF-1 receptors (IGF1Rs) in

161 Insulin receptors (IRs) are expressed in discrete neuron

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

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

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

165 Mice that lack insulin receptors (IRs) throughout development in both n

166 es in diabetic kidney disease (DKD), impairs insulin receptor isoform B-dependent pro-survival insuli

167 a phosphorylation of its tyrosine 987 by the Insulin receptor isoform-A kinase-associated activity in

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

169 rvival insulin signaling by interfering with insulin receptor isoforms binding to caveolin-1 in the P

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

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

172 vation loop that resembles the autoinhibited insulin receptor kinase (IRK).

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

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

175 To this end, we used the liver-specific insulin receptor knockout (LIRKO) mouse, a unique nondie

176 to insulin resistance in the liver-specific insulin receptor knockout (LIRKO) mouse.

177 end, we developed an epidermal skin-specific insulin receptor knockout (SIRKO) mouse, in which the in

178 atic Insr acutely in floxed Insr mice (liver insulin receptor knockout [L-IRKO] + GFP), before adenov

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

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

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

182 chimeric RTKs, termed light-controlled human insulin receptor (LihIR) and light-controlled human MET

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

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

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

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

187 ptor to elucidate its mechanism in eliciting insulin receptor-mediated signaling.

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

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

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

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

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

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

194 Indeed, myeloid-specific knockout of the insulin receptor or bone marrow transplantation of mutan

195 The inferred signal does not require DAF-2/insulin receptor or maintain quiescence of the nearby se

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 However, receptor-level IR (e.g., insulin receptor pathogenic variants, INSR) causes hyper

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

201 e wing disc, while ectopic activation of the insulin receptor, PI3K, or Akt/PKB is sufficient to main

202 We show that GABA(B)-receptor and insulin-receptor play important roles during OSN modulat

203 Insulin receptor plays a central role in skin carcinogen

204 Insulin receptor-related receptor (IRR) is a receptor ty

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

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

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

208 the hypothalamus and decreased expression of insulin receptor signaling genes in adipose (p < 0.05).

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

210 ased postsynaptic differentiation induced by insulin receptor signaling in muscle.

211 Finally, we show that activation of insulin receptor signaling is sufficient to increase neu

212 le growth driven by autonomous modulation of insulin receptor signaling produce corresponding changes

213 o of IRS1 and IRS2 in hepatocytes, impacting insulin receptor signaling via protein kinase B/AKT (AKT

214 otide exchange factor dPix as an effector of insulin receptor signaling.

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

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

217 owth, and their mRNA levels are regulated by insulin receptor signaling.

218 t is essential to understand how insulin and insulin receptor signalling promote cancer progression.

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

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

221 first view of insulin bound to the discrete insulin receptor site 2.

222 distinguish their relative roles, we delete insulin receptor (SMIRKO) or IGF-1 receptor (SMIGF1RKO)

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

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

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

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

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

228 13 bind IL-4 receptors, which signal through insulin receptor substrate (IRS)-2, inducing M2 macropha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 Insulin receptor substrate 1 (IRS1) was overexpressed in

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

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

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

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

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

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

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

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

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

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

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

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

258 3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, there

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 e (Alk) is a receptor tyrosine kinase of the insulin receptor super-family that functions as oncogeni

284 haped (or lambda-shaped) conformation of the insulin receptor, the structural models reconstructed at

285 Pathways linking activation of the insulin receptor to downstream targets of insulin have t

286 tics of this activated fusion protein to the insulin receptor to elucidate its mechanism in eliciting

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

288 Furthermore, LTB4 decreased insulin receptor tyrosine phosphorylation in hepatocytes

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

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

291 Osteoprogenitor-selective ablation of the insulin receptor was induced after ~10 weeks of age in I

292 osolic protein tyrosine kinase domain of the insulin receptor was not affected by ER stress.

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

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

295 5, belongs to a clade of RTKs related to the insulin receptor, which are distinguished by an extracel

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

297 Moreover, extracellular SQSTM1 binds to insulin receptor, which in turn activates a nuclear fact

298 s of IRR by comparing them with those of the insulin receptor, which is its closest homolog but does

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

300 Blockade of insulin receptors (with S961) in the arcuate nucleus, th