ライフサイエンスコーパス: IRS

1 IRS coverage was approximately 90%.

2 IRS developed in 14% (9/64) of the patients, a median of

3 IRS is a feasible method to differentiate disease-specif

4 IRS was defined based on previously proposed criteria.

5 IRS was defined based on previously proposed criteria.

6 IRS was documented in 14% of the SOT recipients with TB.

7 IRS-2 colocalization with tubulin is enhanced upon Taxol

8 Insulin receptor substrate 1 (IRS-1) and IRS-2 are cytoplasmic adaptor proteins that m

9 expression of insulin receptor substrate 1 (IRS-1) phosphorylated at serine residue 312 was more app

10 tion levels of insulin receptor substrate 1 (IRS-1) Tyr(896) and Akt Ser(473) in response to insulin.

11 o-immunoprecipitation of IR, IR substrate 1 (IRS-1), and IGF-1R, and increased IRS-1 and Akt phosphor

12 to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdown enhances the antitumor effec

13 affold protein insulin receptor substrate 1 (IRS-1).

14 se B (AKT) and insulin receptor substrate-1 (IRS-1) in the hypothalamic arcuate was determined.

15 Insulin receptor substrate-1 (IRS-1) is a signaling adaptor protein that interfaces wi

16 mulation TrkA, insulin receptor substrate-1 (IRS-1), INSR (and presumably other proteins) forms a com

17 e receptor and insulin receptor substrate-1 (IRS-1), leading to activation of the PKB/Akt and MAPK/ER

18 ress including insulin receptor substrate-1 (IRS-1), phosphatidyl inositol-3 kinase (PI3K), Mammalian

19 ylation of the insulin receptor substrate-1 (IRS-1).

20 that relies on the IGF receptor substrate-1 (IRS-1).

21 ins, including insulin receptor substrate-1 (IRS-1).

22 of DDT use (non-DDT IRS household, n = 106), IRS village in household with a high likelihood of DDT u

23 e of residence: unsprayed village (n = 175), IRS village in household with a low likelihood of DDT us

24 ely these data support a role for the IGF-1R-IRS-1 pathway in both ALK TKI-sensitive and ALK TKI-resi

25 ylation of the insulin receptor substrate-2 (IRS-2) in macrophages.

26 onducted in all sites, and in December 2014, IRS with the carbamate bendiocarb was initiated in Nagon

27 an exosomal levels of extracted P-serine 312-IRS-1 and P-pan-tyrosine-IRS-1 by ELISA and the ratio of

28 e factor, R) for AD and DM2 and P-serine 312-IRS-1 and R for FTD were significantly different from th

29 IRS-1 by ELISA and the ratio of P-serine 312-IRS-1 to P-pan-tyrosine-IRS-1 (insulin resistance factor

30 nts with AD, exosomal levels of P-serine 312-IRS-1, P-pan-tyrosine-IRS-1, and R were significantly di

31 Compared with no IRS protection, >90% IRS protection reduced preterm birth risk (risk ratio, 0

32 y rate (TPR) were estimated during and after IRS using interrupted time series analyses, controlling

33 reductions in malaria can be sustained after IRS is discontinued.

34 substrate/phosphatidylinositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3

35 ampal response to insulin, caused by altered IRS-1 and PTEN (phosphatase and tensin homologue on chro

36 Although IRS-1 and IRS-2 share significant homology, they regulat

37 These results indicate that although IRS isoforms play divergent roles in the developmental r

38 from 2 studies conducted before and after an IRS campaign in Tororo, Uganda, among HIV-infected pregn

39 Here we identify Nedd4 as an IRS-2 ubiquitin ligase.

40 nificantly lower than the mean SUVmax for an IRS of 2 or more (n = 36; 12.38 +/- 15.02; P < 0.001).

41 The mean SUVmax of PCA and PN for an IRS of less than 2 (n = 26; 2.52 +/- 0.64) was significa

42 ction to protect cancer cells from ROS in an IRS-1-dependent manner.

43 chanism by which signaling through IRS-1 and IRS-2 results in differential outcomes, we assessed the

44 Although IRS-1 and IRS-2 share significant homology, they regulate distinct

45 Insulin receptor substrate 1 (IRS-1) and IRS-2 are cytoplasmic adaptor proteins that mediate the

46 or insulin receptor substrate 1 (IRS-1), and IRS-1 knockdown enhances the antitumor effects of ALK in

47 with this finding, the levels of IGF-1R and IRS-1 are increased in biopsy samples from patients prog

48 s vis a vis insulin but may protect IR-A and IRS-1 from down-regulation thereby evoking sustained and

49 horylation was decreased, p38MAPK, Akt1, and IRS-1 phosphorylation at Ser-307 were increased, togethe

50 CRP with Abeta plaques, tau-like fibrils and IRS-1/P-Tau positive neurons and high mCRP-levels spread

51 cells, tyrosine phosphorylation of INSR and IRS-1 is dependent upon the functional TrkA kinase domai

52 reveal that IQGAP1 is a scaffold for IR and IRS-1 and implicate IQGAP1 as a participant in insulin s

53 show that IQGAP1 associates with both IR and IRS-1 and influences insulin action.

54 sistent with these observations, both IR and IRS-1 co-immunoprecipitated with IQGAP1 from cells.

55 randomly allocated to ITNs only or ITNs and IRS.

56 The Nedd4 and IRS-2 association is also required for maximal activatio

57 Notably, rictor and IRS-1 phosphorylation by p70S6K1 attenuate insulin actio

58 Any IRS protection significantly reduced malaria incidence d

59 hosphate pirimiphos methyl were evaluated as IRS treatments in experimental huts in an area of Benin

60 Given the poor quality of the DDT-based IRS, ready availability of pyrethroids, and susceptibili

61 e may have had an impact on pyrethroid-based IRS.

62 Because IRS-1 is down-regulated in states of insulin resistance

63 han six actions to prepare their home before IRS (e.g., covering water and food) had 40% lower DDT le

64 placental S6K, S6 ribosomal protein, 4E-BP1, IRS-1, Akt, ERK-1/2, and GSK-3.

65 ization, indicating sequestration of aPKC by IRS-1 away from MARK2.

66 (16%), and 97 (17%) women were protected by IRS for 0%, >0% to 90%, and >90% of their pregnancy, res

67 was the proportion of pregnancy protected by IRS.

68 significant added protection from combining IRS and ITNs compared to ITNs alone.

69 ition, CART induced phosphorylation of CREB, IRS, PKB, FoxO1, p44/42 MAPK, and p90RSK in INS-1 (832/1

70 ian levels of DDT and DDE among women in DDT IRS households were 2.6 (IQR: 1.1-6.6) and 8.5 (IQR: 4.7

71 In DDT IRS households, women who reported taking more than six

72 ld with a low likelihood of DDT use (non-DDT IRS household, n = 106), IRS village in household with a

73 ehold with a high likelihood of DDT use (DDT IRS household, n = 100).

74 Defective IRS-1 degradation was due to attenuated expression and p

75 Policy makers should consider deploying IRS in combination with ITNs to control transmission if

76 ly, plasma levels of exosomal neural-derived IRS-1 phosphorylated at serine residue 307 (correspondin

77 lities (P = .03) were more likely to develop IRS, irrespective of serum or CSF cryptococcal antigen t

78 Of 89 SOT recipients, 13 (14%) developed IRS.

79 atients without these risk factors developed IRS compared with 18.8% (6/32) with 1 risk factor, and 5

80 In diabetes, IRS-1 is down-regulated, and cells become resistant to i

81 in the organic nanocomposite layers for each IRS.

82 two pathways involving the actions of either IRS/PI3K/Akt or Grb/Shc/MAPK.

83 ation of Nedd4 with IRS-2, thereby enhancing IRS-2-mediated signalling and cell proliferation induced

84 d AMPKalpha, patient leukocytes also express IRS-1 phosphorylated on Ser(312), Akt phosphorylated on

85 (18)F-IRS accumulation was preferential in the tumor, which wa

86 The uptakes of (18)F-IRS by HCC827 and HCC827 tumors were significantly highe

87 prepare and evaluate a new radiotracer (18)F-IRS for molecular imaging mutant EGF Receptors in vitro

88 experiments showed an accumulation of (18)F-IRS in tumors of HCC827 xenografts.

89 formed to quantify the accumulation of (18)F-IRS in vivo.

90 We also performed (18)F-IRS PET/CT imaging of three patients with NSCLC.

91 (18)F-IRS showed high binding stability and specificity to 19

92 Uptake and efflux of (18)F-IRS were performed with four NSCLC cell lines including

93 ak transmission season, 6 mo after the first IRS.

94 phrin-PI3K binding site and renders PI3K for IRS-1, thereby activating mTORC1.

95 id formulation is now being reintroduced for IRS in a rotational insecticide resistance management pr

96 ranslocation and negated the requirement for IRS-1.

97 We determined variables that pose a risk for IRS and have shown that discontinuation of calcineurin i

98 ouseholds where DDT is likely to be used for IRS, education regarding home preparations may provide a

99 When deltamethrin was used for IRS, incidence rates in the LLIN + IRS arm and the LLIN-

100 When bendiocarb was used for IRS, there was some evidence of additional protection [i

101 y reduced responses to IGF-1 in the IGF-1R-->IRS-2-->PI3K signaling pathway.

102 d responses to insulin signaling in the IR-->IRS-1-->PI3K signaling pathway with greatly reduced resp

103 Despite high IRS coverage and equitable LLIN distribution, poverty wa

104 he intracellular domain of IR display higher IRS-1 phosphorylation, stronger regulation of genes in m

105 tile: OR = 0.26, 95%CI:0.15-0.44); household IRS or high community ITN ownership were not protective.

106 th microtubule-disrupting drugs, identifying IRS-2 as a potential biomarker for the response of breas

107 aphite foil (non-conductive materials) as in IRS, and is the first system capable of being used under

108 volvement of the microtubule cytoskeleton in IRS-dependent signaling.

109 l assessments were made in four districts in IRS and non-IRS villages.

110 The abundance of sand flies in IRS and non-IRS villages was significantly different at

111 DDT/DDE exposure in pregnant women living in IRS communities.

112 suggest that whilst programmed reductions in IRS-1 are associated with increased levels of miR-126 an

113 VSMC dedifferentiation, was up-regulated in IRS-1(-/-) mice, and the differentiation inducer myocard

114 edly triggers IRS-1 downregulation, inactive IRS-1 accumulated in mTORC2-disrupted cells.

115 Proximal IGF-1R signaling events, including IRS tyrosine phosphorylation and recruitment of PI3K, ar

116 activity of PI3K/AKT, but it also increased IRS-1 activity.

117 bstrate 1 (IRS-1), and IGF-1R, and increased IRS-1 and Akt phosphorylation accompany receptor activat

118 independent mechanisms, including increased IRS-1 protein degradation.

119 ect of proteasome inhibitors on IL-4-induced IRS-2 phosphorylation.

120 as a key negative regulator of IL-4-induced IRS-2 signaling and M2 differentiation.

121 peutically manipulated to limit IL-4-induced IRS-2 signaling and polarization of M2 macrophages in al

122 activated the JNK/TNF-alpha pathway, induced IRS-1 phosphorylation at multiple serine residues, and i

123 binding, and enhances IGF-I receptor-induced IRS-2 tyrosine phosphorylation.

124 and indoor residual spraying of insecticide (IRS) are the primary vector control interventions used t

125 by indoor residual spraying of insecticide (IRS).

126 We present new IGF-IR/IRS-targeted agents (NT compounds) that promote inhibito

127 eptin resistance by an improvement of the IR/IRS-1/Akt and JAK2/STAT3 pathways in the hypothalamus.

128 treat analysis, mean PfPR was 13% in the ITN+IRS arm and 26% in the ITN only arm, odds ratio = 0.43 (

129 rate was non-significantly lower in the ITN+IRS arm than in the ITN only arm, rate ratio = 0.17 (95%

130 Dwellings in the ITN+IRS arm were sprayed with two rounds of bendiocarb in 20

131 used for IRS, incidence rates in the LLIN + IRS arm and the LLIN-only arm were similar, with the IRS

132 nal lymph nodes, age less than 10 years, low IRS group, and embryonal histology.

133 Mechanistically, IRS-1 deficiency promotes Janus kinase/signal transducer

134 In PCA sections (n = 31), median IRS was 3, median staining intensity was strong, and med

135 Nedd4 monoubiquitinates IRS-2, which promotes its association with Epsin1, a ubi

136 Compared with no IRS protection, >90% IRS protection reduced preterm birt

137 The abundance of sand flies in IRS and non-IRS villages was significantly different at 1 mo post-IR

138 s were made in four districts in IRS and non-IRS villages.

139 e cytoskeleton contributes to IRS-2- but not IRS-1-mediated activation of AKT by IGF-1.

140 substrate-1 at Ser302 (IRS-1(S302)) but not IRS-2, by insulin was markedly increased in CCR5 and CCL

141 tubule cytoskeleton may facilitate access of IRS-2 to downstream effectors such as AKT.

142 ited decreased phosphorylation/activation of IRS-1 and AKT following stimulation by insulin, insulin-

143 Insulin's activation of IRS/PI3K/Akt results in mostly antiatherogenic actions,

144 ibution in three sites, with the addition of IRS at one of these sites.

145 ria for some indicators, but the addition of IRS at the highest transmission site was associated with

146 ling-1, implicating increased degradation of IRS-1 as an underlying mechanism.

147 Here we show that deletion of IRS-1 expression in VSMCs in non-diabetic mice results i

148 Discontinuation of IRS in an area with historically high transmission inten

149 the 4-18 months following discontinuation of IRS, absolute TPR values increased by an average of 3.29

150 larly, the phosphotyrosine-binding domain of IRS-1 mediates a direct interaction with the C-terminal

151 ings, NT compounds led to the elimination of IRS proteins and evoked cell death.

152 By the elimination of IRS proteins, such agents should prevent acquisition of

153 egulation of the relative gene expression of IRS-1, PI3K and Akt in the insulin signaling pathway, wh

154 e is that our data reveal that expression of IRS-2 sensitizes breast carcinoma cells to apoptosis in

155 These findings illuminate a new function of IRS-1: that of maintaining cells in their normal, differ

156 insulin resistance, including inhibition of IRS-1 mRNA levels and activation of gluconeogenesis-rela

157 Inhibition of IRS-2 action by 30 muM SSRI was associated with a marked

158 se findings implicate SSRIs as inhibitors of IRS protein function and insulin action through the acti

159 Here we show that loss of IRS signaling prevented the physiological suppression of

160 ude that Nedd4-induced monoubiquitination of IRS-2 enhances IGF signalling and mitogenic activity.

161 for activity, we show that overexpression of IRS-1 reduces the phosphorylation of MARK2 and enhances

162 r(P)) and serine phosphorylation (Ser(P)) of IRS-2 after IL-4 stimulation.

163 ably through the negative phosphorylation of IRS-1 on Ser-1101.

164 et)CCL5, abolished the de-phosphorylation of IRS-1(S302) and insulin signal activation.

165 owed that insulin-induced phosphorylation of IRS-1, Akt, and eNOS was significantly decreased in ZF r

166 via the inhibitory serine phosphorylation of IRS-1, notably on serine 1101 (Ser-1101).

167 is dependent upon serine phosphorylation of IRS-2.

168 We hypothesized that negative regulation of IRS-2 activity after IL-4 stimulation is dependent upon

169 ere, we describe a new negative regulator of IRS-1, the p90 ribosomal S6 kinase (RSK).

170 conferred a 19-fold increase in the risk of IRS (P=0.01).

171 tly associated with 5-fold increased risk of IRS in transplant recipients with cryptococcosis.

172 74-27) were associated with a higher risk of IRS.

173 To determine the role of IRS isoforms in mediating the hypertrophic and metabolic

174 The addition of three rounds of IRS at ~6-mo intervals in Nagongera was followed by clea

175 Rounds of IRS were delivered approximately every 6 months from Feb

176 onocytes displayed greater ubiquitination of IRS-2 and lower M2 polarization than allergic monocytes

177 phosphorylation, increased ubiquitination of IRS-2, and enhanced M2 gene expression.

178 of SOCS3 had no effect on ubiquitination of IRS-2.

179 of SOCS1 inhibited ubiquitin accumulation on IRS-2, although siRNA knockdown of SOCS3 had no effect o

180 Data on IRS and ITN coverage, household demographics and socio-e

181 effects of a post-weaning obesogenic diet on IRS-1 are mediated by miR-126 independent mechanisms, in

182 apsanthin was the most abundant at the other IRS.

183 serine phosphatase activity increased Ser(P)-IRS-2 and decreased Tyr(P)-IRS-2 leading to reduced M2 g

184 ream of TORC1, resulted in diminished Ser(P)-IRS-2 and prolonged Tyr(P)-IRS-2 as well.

185 in downstream of TORC1, enhanced both Tyr(P)-IRS-2 and increased expression of all four M2 genes.

186 diminished Ser(P)-IRS-2 and prolonged Tyr(P)-IRS-2 as well.

187 increased Ser(P)-IRS-2 and decreased Tyr(P)-IRS-2 leading to reduced M2 gene expression (CD200R, CCL

188 by reducing the expression of total IRS-1, p-IRS-1 (tyr632), and p-AKT (ser473); it also activates th

189 n in endothelial cells and neurons through p-IRS-1, p-Tau and p-ERK1/2-which was blocked following pr

190 This inhibitory synapse parallels IRS's inhibition of the microcircuit's RS motor neurons.

191 4 membrane translocation and reduced phospho-IRS-1(S302) through AMPKalpha-S6 Kinase.

192 th the level of the Ser(1100)-phosphorylated IRS-2 protein in metastatic melanoma tissues.

193 Moreover, recombinant RSK phosphorylated IRS-1 C-terminal fragment on Ser-1101, which was prevent

194 ) showed that RSK selectively phosphorylates IRS-1 on Ser-1101.

195 serine residues, and inhibited physiological IRS-1pTyr in mature cultured hippocampal neurons.

196 were performed in three districts, and post-IRS surveys were performed in eight districts.

197 The mean residual concentration of DDT post-IRS was 0.37 g ai/m(2); 84.9% of walls were undersprayed

198 ges was significantly different at 1 mo post-IRS only.

199 s were measured: pre-IRS and 1 and 3 mo post-IRS.

200 tuberculosis-associated posttransplantation IRS.

201 Pre-IRS surveys were performed in three districts, and post-

202 Vector densities were measured: pre-IRS and 1 and 3 mo post-IRS.

203 The majority (329 of 360, 91.3%) of pre-IRS samples had residual DDT concentrations of <0.1 g ai

204 a rapid increase in malaria morbidity to pre-IRS levels.

205 Proteasomal inhibition prolonged IRS-2 tyrosine phosphorylation, increased ubiquitination

206 ound that siRNA knockdown of SOCS1 prolonged IRS-2 tyrosine phosphorylation and enhanced M2 different

207 the absence of AA, insulin can still promote IRS-1 Ser-1101 phosphorylation by other kinases that rem

208 d the limited protection given by pyrethroid IRS and LLINs suggest that it may be necessary to enhanc

209 valuates the protective effect of pyrethroid IRS and ITNs in relation to risk factors for malaria bas

210 ow cytometry and confocal imaging with QD620-IRS further demonstrated that binding specifically to HC

211 Nedd4 recruits IRS-2 to the membrane, probably through promoting Epsin1

212 t reduce Akt phosphorylation despite reduced IRS-1 signaling.

213 f IKKepsilon activity, but not TBK1, reduced IRS-1(Ser307) phosphorylation and insulin and leptin res

214 Surprisingly, tumors with reduced IRS-1 staining in a human lung adenocarcinoma tissue mic

215 of Sirt1 to directly deacetylate and repress IRS-1 function.

216 frica with widespread pyrethroid resistance, IRS using alternative insecticide formulations may be ne

217 and aPKC with the insulin-regulated scaffold IRS-1.

218 +/- 14.24%, and median immunoreactive score (IRS) was 1.

219 n of insulin response substrate-1 at Ser302 (IRS-1(S302)) but not IRS-2, by insulin was markedly incr

220 and a segment of the inverted repeat short (IRS)/unique short (US) region.

221 istance and to provide control with a single IRS application in countries with long transmission seas

222 ring (DRS) and indirect resistive sintering (IRS).

223 Sixteen IRS (Intergroup Rhabdomyosarcoma Study) III and IV patie

224 ished previously that infrared spectroscopy (IRS) can be used to identify periodontitis-specific mole

225 Indoor residual spraying (IRS) and long-lasting insecticidal nets (LLINs) are the

226 l nets (LLINs) and indoor residual spraying (IRS) have contributed substantially to reductions in the

227 Although indoor residual spraying (IRS) is an effective tool for malaria control, its use c

228 Indoor residual spraying (IRS) is used to control visceral leishmaniasis (VL) in I

229 Indoor residual spraying (IRS) is widely used for malaria transmission control in

230 Indoor residual spraying (IRS) occurred in half of the villages.

231 ed nets (ITNs) and indoor residual spraying (IRS) of houses provide effective malaria transmission co

232 gnated nets and/or indoor residual spraying (IRS) of insecticide.

233 n combination with indoor residual spraying (IRS) with a pyrethroid (deltamethrin) insecticide in the

234 ated nets (LLINs), indoor residual spraying (IRS), and artemisinin combination therapies (ACTs).

235 ted nets (ITN) and indoor residual spraying (IRS).

236 eno peppers at intermediate ripening stages (IRS) are typically discarded at the packinghouse because

237 ts derivative intermediate resistive states (IRSs) of nanocomposite memory systems have not been clea

238 nt reversed inflammatory cytokine-stimulated IRS-1 serine phosphorylation, increased insulin signalin

239 lation, and inhibition of insulin-stimulated IRS-1 tyrosine phosphorylation and AKT2 phosphorylation.

240 psilon, and impairment of insulin-stimulated IRS-2 signaling.

241 Insulin receptor substrate (IRS) 2 as intermediate docking platform transduces the i

242 e critical nodes insulin receptor substrate (IRS) and phosphatidylinositol 3-kinase (PI3K), exhibit d

243 osphorylation of insulin receptor substrate (IRS) proteins at Ser sites that inhibit insulin and IGF-

244 The insulin receptor substrate (IRS) proteins serve as essential signaling intermediates

245 0-24 h increased insulin receptor substrate (IRS)-1 phosphorylation at Ser-307, decreased protein lev

246 ation, increased insulin receptor substrate (IRS)-1 serine 1101 phosphorylation, and inhibition of in

247 osphorylation of insulin receptor substrate (IRS)-1/2 by IGF-I receptor tyrosine kinase is essential

248 derived from the insulin receptor substrate (IRS)-2 and the cell-cycle regulator CDC25b.

249 osphorylation of insulin receptor substrate (IRS)-2 protein and the activation of its downstream targ

250 h signal through insulin receptor substrate (IRS)-2, inducing M2 macrophage differentiation.

251 P)-serine-type 1 insulin receptor substrate (IRS-1) and less P-tyrosine-IRS-1.

252 Surprisingly, IRS proteins were highly expressed, in contrast to a str

253 Surprisingly, IRS-1 phosphorylation was not diminished in Y325F L-cell

254 immune reconstitution inflammatory syndrome (IRS) in solid-organ transplant (SOT) recipients are not

255 ccurrence of immune reconstitution syndrome (IRS) in solid organ transplant (SOT) recipients with cry

256 Here we demonstrate that Tax-IRS is driven by the transcriptional activity of NF-kapp

257 It has been assumed that IRS-1 promotes tumor growth through its ability to activ

258 oratory analyses support the hypothesis that IRS may significantly reduce malaria and preterm birth r

259 d by microtubule disruption, indicating that IRS-2 requires the microtubule cytoskeleton at the level

260 as detected in this species in 2004, and the IRS program switched to carbamate bendiocarb, has now be

261 ly reduced tumor burden, most notably in the IRS-1-deficient group.

262 apid dephosphorylation and activation of the IRS kinase GSK3beta.

263 ll VEGFR2 induces feedback activation of the IRS/MAPK signaling cascade.

264 In AT, analysis of the IRS/PI3-K/AKT pathway signaling components identified on

265 gy that can be selectively inhibited via the IRS/PI3K/Akt cascade in diabetes.

266 it insulin's antiatherogenic actions via the IRS/PI3K/Akt pathway.

267 and the LLIN-only arm were similar, with the IRS providing no additional protection [incidence rate r

268 anocomposite memory devices with NDR and the IRSs under various temperature conditions.

269 that the localized current pathways for the IRSs are attributed to trapping/de-trapping at the deep

270 ors at various temperature conditions in the IRSs and telegraphic noise in NDR indicate the localized

271 sand flies, the continued use of DDT in this IRS program is questionable.

272 and heat-processed Jalapeno peppers at three IRS (brown, 50% red, and 75% red).

273 celerates zebrafish embryonic growth through IRS-2 in vivo.

274 airs hippocampal response to insulin through IRS-1 and PTEN dysregulation and suggest that, in Alzhei

275 S6K signaling regulates Akt largely through IRS-independent means with little effect upon physiologi

276 ate the mechanism by which signaling through IRS-1 and IRS-2 results in differential outcomes, we ass

277 retrospectively and correlated with the TKTL IRS using Kaplan-Meier and Cox regression analyses.

278 The effect is likely to be attributable to IRS providing added protection to ITN users as well as c

279 tact microtubule cytoskeleton contributes to IRS-2- but not IRS-1-mediated activation of AKT by IGF-1

280 in 2012 to characterize prenatal exposure to IRS insecticides and exposures' impacts on child health

281 ignaling by reducing the expression of total IRS-1, p-IRS-1 (tyr632), and p-AKT (ser473); it also act

282 ated serine sites, which supposedly triggers IRS-1 downregulation, inactive IRS-1 accumulated in mTOR

283 ceptor substrate (IRS-1) and less P-tyrosine-IRS-1.

284 atio of P-serine 312-IRS-1 to P-pan-tyrosine-IRS-1 (insulin resistance factor, R) for AD and DM2 and

285 racted P-serine 312-IRS-1 and P-pan-tyrosine-IRS-1 by ELISA and the ratio of P-serine 312-IRS-1 to P-

286 levels of P-serine 312-IRS-1, P-pan-tyrosine-IRS-1, and R were significantly different 1 to 10 yr bef

287 h limited use in the interim where no viable IRS alternatives exist.

288 tudy conducted in North-West Tanzania, where IRS has been conducted since 2007 and universal coverage

289 da with historically high transmission where IRS was discontinued after a 4-year period followed by u

290 studies were undertaken to determine whether IRS-1 is functioning constitutively to maintain VSMCs in

291 Furthermore, GRB10 associated with IRS-2, NEDD4.2 (an E3-ubiquitin ligase), IL-4Ralpha, and

292 P = .02) were independently associated with IRS.

293 pitation, we found that SOCS1 complexes with IRS-2 at baseline, and this association increased after

294 iation of phosphatidylinositol 3-kinase with IRS-1, were significantly decreased.

295 hway increases the association of Nedd4 with IRS-2, thereby enhancing IRS-2-mediated signalling and c

296 r after diagnosis was 33.3% in patients with IRS and 17.2% in those without IRS (P=0.31).

297 bserved in 15.4% (2/13) of the patients with IRS compared with 2.6% (2/76) of those without IRS (P =

298 ional analyses revealed that Ser-1101 within IRS-1 falls into the consensus motif of RSK.

299 S compared with 2.6% (2/76) of those without IRS (P = .07).

300 patients with IRS and 17.2% in those without IRS (P=0.31).