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1 sozyme (RCAM-lysozyme), a well characterized insulin receptor substrate.
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
13 th decreased levels of serine-phosphorylated insulin receptor substrate 1 (IRS-1), a molecule implica
14 ylation of JNK and serine phosphorylation of insulin receptor substrate 1 (IRS-1), along with inhibit
15 -1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdow
16 ling (SOCS3) in muscle, which led to loss of insulin receptor substrate 1 (IRS-1), thereby impairing
17 pogenesis, we examined the effect of BMP7 in insulin receptor substrate 1 (IRS-1)-deficient brown pre
18 in spite of decreased signaling through the insulin receptor substrate 1 (IRS-1)-phosphoinositide (P
22 e peptides (dilp2-3,5(-/-)) and mice lacking insulin receptor substrate 1 (Irs1(-/-)), and two indepe
23 KD cells reduced tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) (pY(896)) and phosph
24 sistance because of enhanced skeletal muscle insulin receptor substrate 1 (IRS1) and Akt phosphorylat
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
30 based gene expression profiling we found the insulin receptor substrate 1 (IRS1) gene as one of the m
32 lele of rs2943641 near the gene encoding for insulin receptor substrate 1 (IRS1) has been associated
35 e reverse-phase protein array, we found that insulin receptor substrate 1 (IRS1) is the most highly u
37 kinase A (PKA)-dependent phosphorylation of insulin receptor substrate 1 (IRS1) on tyrosine residues
39 SHH-treated CGNPs showed increased levels of insulin receptor substrate 1 (IRS1) protein, which was a
41 dent receptor autophosphorylation as well as insulin receptor substrate 1 (IRS1) tyrosine phosphoryla
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
51 of HNF-4A gene (rs2144908 and rs1884614) and insulin receptor substrate 1 (rs1801278) are significant
52 the level of the insulin receptor, increased insulin receptor substrate 1 (Ser-312), and decreased Ak
53 884614, OR=2.44, CI=1.42-4.48, P=0.002), and insulin receptor substrate 1 AA+AG (rs1801278, OR=2.71,
54 a mouse model that harbors hepatic-specific insulin receptor substrate 1 and 2 deletions (double kno
55 port a non-canonical interaction between the insulin receptor substrate 1 and certain oncogenic varia
56 e, with dramatically decreased expression of insulin receptor substrate 1 and glucose transporter 4 i
57 tenuates insulin signaling and expression of insulin receptor substrate 1 and phosphoinositide 3-kina
58 because of the impaired interaction between insulin receptor substrate 1 and the p85alpha subunit of
59 ed protein kinase (AMPK), and phosphorylated insulin receptor substrate 1 at serine 307 (IRS1-s307).
61 found greater inhibitory phosphorylation of insulin receptor substrate 1 in each brain region examin
62 y 29% +/- 13% and phosphorylation of Akt and insulin receptor substrate 1 increased by 35% +/- 9% and
63 eficient in cyclin D2 (D2KO) with either the insulin receptor substrate 1 knockout (IRS1KO) mice or t
64 sses forkhead box O3, B-cell lymphoma 2, and insulin receptor substrate 1 mRNAs in the cocultured SMC
65 vity and reduced glucocorticoid induction of insulin receptor substrate 1 phosphorylation at serine 3
66 duced Jun NH2-terminal kinase activation and insulin receptor substrate 1 serine phosphorylation in v
67 inase activity by 183 +/- 6% (p = 0.003) and insulin receptor substrate 1 tyrosine phosphorylation by
69 ith these changes, serine phosphorylation of insulin receptor substrate 1 was reduced, and Akt activa
70 scle expression of insulin receptor beta and insulin receptor substrate 1 were down-regulated 2-fold
71 s to stimulate YXXM phosphorylation of IRS1 (insulin receptor substrate 1) required for PI3K/AKT acti
72 egulin, and glucose metabolism-involved gene insulin receptor substrate 1), and 27 genes in the nondi
73 sduction by impairing the phosphorylation of insulin receptor substrate 1, a protein that couples act
75 es and, in some cells, reduced expression of insulin receptor substrate 1, and both IGF1 and insulin
76 ta-catenin, c/EBPalpha,c-Myc, cyclin D1, and insulin receptor substrate 1, and cell growth/survival.
77 syl phosphorylation of the insulin receptor, insulin receptor substrate 1, and their downstream casca
78 phorylation of type I IGF receptor (IGF-IR), insulin receptor substrate 1, phosphatidylinositol 3-kin
79 rylation in muscle may explain the increased insulin receptor substrate 1, PI3K, and ERK phosphorylat
80 stabilization of a second messenger protein, insulin receptor substrate 1, that mediates PI 3-kinase-
81 s associated with reduced insulin-stimulated insulin receptor substrate 1- (IRS-1-) and IRS-2-associa
85 that PKC activation differentially inhibited insulin receptor substrate 1/2 (IRS1/2) signaling of ins
86 as evidenced by increased phosphorylation of insulin receptor substrate 1/2 and enhanced ERK/Akt acti
88 stance is a hallmark of type 2 diabetes, and insulin receptor substrates 1 and 2 (IRS1 and IRS2) are
90 insulin signaling through phosphorylation of insulin-receptor substrates 1 and 2 at sites that interf
92 owed that E2 influenced on protein levels of insulin receptor substrate-1 (IRS-1) and impaired insuli
93 ugh both proteasome-dependent degradation of insulin receptor substrate-1 (IRS-1) and inhibition of t
94 owing to the deletion of the genes encoding insulin receptor substrate-1 (Irs-1) and Irs-2 (referred
95 IGF-1 stimulates tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-2 and their
97 igands for ALK and that upon ALK activation, insulin receptor substrate-1 (IRS-1) and other substrate
98 ylation of c-Jun N-terminal kinase (JNK) and insulin receptor substrate-1 (IRS-1) at Ser-307 were inc
99 I) 3-kinase/Akt signaling by phosphorylating insulin receptor substrate-1 (IRS-1) at Ser-636/639.
101 ke growth factor receptor (IGF-IR) or of the insulin receptor substrate-1 (IRS-1) genes in animals ca
102 activity of PI3K/protein kinase B (AKT) and insulin receptor substrate-1 (IRS-1) in the hypothalamic
105 ses a route that promotes phosphorylation of insulin receptor substrate-1 (IRS-1) on Tyr(989), a cano
106 EFs and several other cell lines requires an insulin receptor substrate-1 (IRS-1) phosphorylated on t
109 showed that IGF-I, IGF-IR mRNAs, and phospho-insulin receptor substrate-1 (IRS-1) protein were decrea
110 decreased insulin signaling at the level of insulin receptor substrate-1 (IRS-1) tyrosine phosphoryl
112 of IGF-I-induced cell cycle progression and insulin receptor substrate-1 (IRS-1) tyrosine phosphoryl
114 phoinositide-3 kinase (PI3K) associated with insulin receptor substrate-1 (IRS-1) was attenuated (P <
116 a-catenin binds to and co-localizes with the insulin receptor substrate-1 (IRS-1), a docking protein
117 During insulin or NGF stimulation TrkA, insulin receptor substrate-1 (IRS-1), INSR (and presumab
118 tyrosine phosphorylation of the receptor and insulin receptor substrate-1 (IRS-1), leading to activat
119 ith cardiac hypertrophy and stress including insulin receptor substrate-1 (IRS-1), phosphatidyl inosi
121 -high cells, and this enhanced expression of insulin receptor substrate-1 (IRS-1), the principle intr
130 ced phosphorylation of insulin receptor (IR)/insulin receptor substrate-1 (IRS-1)/Akt pathway in the
132 within the phosphotyrosine-binding domain of insulin receptor substrate-1 (IRS-PTB), we have used NMR
133 -growth factor-1 signaling pathways, such as insulin receptor substrate-1 (IRS1) and IRS2, differenti
134 ide explained by attenuation of an mTORC1-to-insulin receptor substrate-1 (IRS1) feedback and reduced
139 and phosphoinositide 3-kinase decreased, and insulin receptor substrate-1 307 phosphorylation increas
141 Absence of LAR enhanced phosphorylation of insulin receptor substrate-1 and insulin receptor substr
143 ling and known feedback mechanisms affecting insulin receptor substrate-1 and phosphatidylinositol 3-
144 TNF-alpha-mediated serine phosphorylation of insulin receptor substrate-1 and protein tyrosine phosph
145 it with the IGF-I receptor (IGF-IR) effector insulin receptor substrate-1 and with ErbB3, implicating
147 insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 as well as Akt phosphorylat
148 We now show that mTOR inhibition induces insulin receptor substrate-1 expression and abrogates fe
149 effects including an mTOR-dependent loss in insulin receptor substrate-1 expression leading to feedb
150 sen, an antisense oligonucleotide preventing insulin receptor substrate-1 expression, inhibited corne
151 2 interacts with and directly phosphorylates insulin receptor substrate-1 in cardiomyocytes, causing
152 phosphorylation of the insulin receptor and insulin receptor substrate-1 in response to insulin incr
154 o insulin action, and 3) basal inhibition of insulin receptor substrate-1 may decrease insulin action
155 (8.4-fold, P < 0.01), paralleled by reduced insulin receptor substrate-1 mRNA expression (-0.7-fold,
156 d expression of the key downstream messenger insulin receptor substrate-1 phosphorylated at serine re
157 mRNA of the DUSP-5 and 2) increases hepatic insulin receptor substrate-1 phosphorylation at serine 6
159 significant increases in glucose metabolism, insulin receptor substrate-1, and Akt activity in muscle
163 nase, enhances the serine phosphorylation of insulin receptor substrate-1, and increases the expressi
164 insulin signaling cascade (insulin receptor, insulin receptor substrate-1, p85, phosphatidylinositol
165 on of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sen
166 rylation of insulin receptor substrate-1 and insulin receptor substrate-1-associated phosphoinositide
172 -induced phosphorylation of Akt, ERK1/2, and insulin receptor substrate-1/2 was decreased and followe
173 ermined the kinetics of dephosphorylation of insulin receptor substrate-1/2, Akt, and ERK1/2, phospho
174 ays: one mediated by STAT6, and the other by insulin receptor substrates-1 and -2 via activation of P
178 ubsequent 52% decrease in insulin-stimulated insulin receptor substrate 2 (IRS-2) tyrosine phosphoryl
179 that promotes beta-cell growth and survival, insulin receptor substrate 2 (IRS-2), is a member of a f
180 insulin-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2), whereas it had min
181 teins involved in insulin signaling, such as insulin receptor substrate 2 (IRS2) and glucose transpor
182 3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, there
183 component of all types of diabetes, and the insulin receptor substrate 2 (IRS2) branch of signaling
186 s, proliferation, and survival by increasing insulin receptor substrate 2 (IRS2) levels and identify
188 s is sufficient to enhance the expression of insulin receptor substrate 2 (IRS2) to levels observed i
189 2)-associated binding proteins 1-3 (GAB1-3), insulin receptor substrate 2 (IRS2), docking protein 1 (
190 mice lacking insulin signaling intermediate insulin receptor substrate 2 (IRS2), we confirmed that h
191 The study also provides strong evidence that insulin receptor substrate 2 (Irs2), which is known to h
192 ronic morphine-induced downregulation of the insulin receptor substrate 2 (IRS2)-thymoma viral proto-
193 Moreover, miR-33a and -b also target the insulin receptor substrate 2, an essential component of
194 results in enhanced IR signaling through the insulin receptor substrate 2-AKT pathway in beta-cells a
196 related with tyrosine phosphorylation of the insulin receptor substrate-2 (IRS-2) in macrophages.
199 to abused drugs decreases the expression of insulin receptor substrate-2 (IRS-2; a protein involved
200 of sarcomas and found a marked induction of insulin receptor substrate-2 (IRS2) and phosphorylated A
201 hat mice heterozygous for a null mutation in insulin receptor substrate-2 (Irs2) display a 17% increa
202 3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstr
206 ing through direct and indirect induction of insulin receptor substrate-2 (Irs2), an essential insuli
207 ysis occurs normally in B cells deficient in insulin receptor substrate-2 or the p85alpha subunit of
208 The hepatic mRNA level of the HIF-2 target insulin receptor substrate-2 was higher, whereas that of
209 lts in decreased tyrosine phosphorylation of insulin receptor substrate-2 with impeded insulin signal
210 n key insulin-signaling molecules, including insulin receptor substrate-2, and substrate metabolism t
211 ic screen of HD, we found that activation of insulin receptor substrate-2, which mediates the signali
212 ximately 40% reduction in insulin-stimulated insulin receptor substrate-2-associated phosphatidylinos
215 hyperinsulinemic-euglycemic clamp and muscle insulin receptor substrate and Akt phosphorylation demon
218 ased brain glucose uptake, activation of the insulin receptor substrate and of the PI3K/Akt signaling
219 phosphorylation nor the interaction between insulin receptor substrate and phosphatidylinositide 3-k
221 teosomal degradation of the docking protein, insulin receptor substrate, and enhanced signaling throu
222 ugh serine phosphorylation and inhibition of insulin receptor substrate by the downstream effector of
226 easured the life span of mice lacking either insulin receptor substrate (IRS) 1 or 2, the major intra
228 IS/TOR network, including the critical nodes insulin receptor substrate (IRS) and phosphatidylinosito
231 ammatory cytokines induce phosphorylation of insulin receptor substrate (IRS) proteins at Ser sites t
234 ciated with reduced expression of both major insulin receptor substrate (IRS) proteins, IRS-1 and IRS
235 naling and the extent to which alteration of insulin receptor substrate (IRS) signaling modulates bet
238 CS)3 deficiency increases insulin-stimulated insulin receptor substrate (IRS)-1 and -2 phosphorylatio
239 ficiency suppressed the up-regulation of the insulin receptor substrate (IRS)-1 and IRS-2 and thereby
241 l line decreased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2 in response
242 o delayed and impaired activation of hepatic insulin receptor substrate (IRS)-1 and IRS-2 signaling,
243 xpression of major IGF signaling components, insulin receptor substrate (IRS)-1 and IRS-2, an effect
244 of mRNAs for insulin receptor (IR)A and IRB; insulin receptor substrate (IRS)-1 and IRS-2; phosphoino
245 g SOCS3 and via SOCS3-mediated inhibition of insulin receptor substrate (IRS)-1 and possibly AMPK in
248 association between genetic variants of the insulin receptor substrate (IRS)-1 gene, platelet functi
249 xamine the role of serine phosphorylation of insulin receptor substrate (IRS)-1 in mediating fat-indu
250 Ad-GLP-1 treatment increased basal levels of insulin receptor substrate (IRS)-1 in the liver and acti
251 in (10(-8) to 10(-7) m) for 0-24 h increased insulin receptor substrate (IRS)-1 phosphorylation at Se
252 yotubes, dexamethasone (> or = 24 h) reduced insulin receptor substrate (IRS)-1 protein and PI3K/Akt
253 ure to NO donor or iNOS transfection reduced insulin receptor substrate (IRS)-1 protein expression wi
254 tein kinase (PKC)theta activation, increased insulin receptor substrate (IRS)-1 serine 1101 phosphory
256 rough inactivation of S6K1, stabilization of insulin receptor substrate (IRS)-1, and increased signal
257 increased insulin receptor signaling, i.e., insulin receptor substrate (IRS)-1, insulin receptor pho
258 raised insulin-like growth factor-1 (IGF-1), insulin receptor substrate (IRS)-1, vascular endothelial
259 is, p85alpha mRNA and protein expression and insulin receptor substrate (IRS)-1-associated PI 3-kinas
261 betes reduced basal insulin receptor kinase, insulin receptor substrate (IRS)-1/2-associated phosphat
262 sulin-like growth factor receptor-1 (IGF-1R)/insulin receptor substrate (IRS)-1/Akt pathway with ERal
263 the insulin receptor catalytic activity and insulin receptor substrate (IRS)-1/IRS-2 dephosphorylati
264 educed strength of insulin signaling via the insulin receptor substrate (IRS)-1/phosphatidylinositol
265 -restricted phosphopeptides derived from the insulin receptor substrate (IRS)-2 and the cell-cycle re
266 bited insulin-induced Tyr phosphorylation of insulin receptor substrate (IRS)-2 protein and the activ
268 13 bind IL-4 receptors, which signal through insulin receptor substrate (IRS)-2, inducing M2 macropha
269 ic glucose production and insulin-stimulated insulin receptor substrate (IRS)-2-associated phosphatid
271 ikely caused by, direct dephosphorylation of insulin receptor substrate (IRS)1/2 in the liver, accomp
273 Pituitaries responded to insulin through insulin receptor substrate (IRS)2 but not IRS1, whereas
274 ort an altered interrelationship between the insulin receptor substrate (IRS-1) and Akt/mTOR pathway
275 ociation with more phospho (P)-serine-type 1 insulin receptor substrate (IRS-1) and less P-tyrosine-I
277 ceptors (IR) resulting in phosphorylation of insulin receptor substrates (IRS) inducing activation of
278 e effects are mediated, at least in part, by insulin receptor substrates (IRS), one of which is insul
280 ut displayed severely blunted signalling via insulin-receptor substrate (IRS) proteins, key mediators
282 ne kinase (MCK)-Cre to disrupt expression of insulin receptor substrates Irs1 and Irs2 in mouse skele
283 resistin increased serine phosphorylation of insulin receptor substrate (IRS1) through the activation
285 This is the result of downregulation of the insulin receptor substrates, IRS1 and IRS2, which become
287 gnaling for energy uptake and growth through insulin receptor substrates (IRSs), which interact with
288 ion levels in the brain for two transcripts, insulin receptor substrate p53 (IRSp53) and Calsenilin.
290 improved insulin signal transduction via the insulin receptor substrate-phosphatidylinositol-3-hydrox
291 hese hormones induces cell signaling via the insulin receptor substrate/phosphatidylinositol 3-kinase
292 pathways in rodent beta-cells, including the insulin receptor substrate/phosphatidylinositol-3 kinase
293 ing selectively in endothelial cells via the insulin receptor substrate/PI3K/Akt pathway to reduce th
295 ess at least two Tiam1-interacting proteins, insulin receptor substrate protein 53 kDa (IRSp53) and s
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)
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