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1 sozyme (RCAM-lysozyme), a well characterized insulin receptor substrate.
2                       Both downregulation of insulin receptor substrate 1 (IRS-1) and dominant-negati
3                                              Insulin receptor substrate 1 (IRS-1) and IRS-2 are cytop
4              Furthermore, we showed that the insulin receptor substrate 1 (IRS-1) expression and insu
5               Furthermore, the expression of insulin receptor substrate 1 (IRS-1) phosphorylated at s
6                    Insulin increased AKT and insulin receptor substrate 1 (IRS-1) phosphorylation, sy
7                                              Insulin receptor substrate 1 (IRS-1) plays a key role in
8 ation factor 4E (eIF4E) S209, Smad2 S465/67, insulin receptor substrate 1 (IRS-1) S612, mitogen-activ
9 egative feedback loop imposed on the IGF-IR- insulin receptor substrate 1 (IRS-1) signaling complex,
10 (SOCS3) show lower phosphorylation levels of insulin receptor substrate 1 (IRS-1) Tyr(896) and Akt Se
11               Similarly, the docking protein insulin receptor substrate 1 (IRS-1) was down-regulated
12                In this report, we identified insulin receptor substrate 1 (IRS-1), a critical mediato
13 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
19 n receptor substrates (IRS), one of which is insulin receptor substrate 1 (IRS-1).
20 et of rapamycin)-mediated phosphorylation of insulin receptor substrate 1 (IRS-1).
21  (IGF-I) signal through the scaffold protein insulin receptor substrate 1 (IRS-1).
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
25                These effects are mediated by insulin receptor substrate 1 (IRS1) and IRS2, which also
26  is critical for the membrane recruitment of insulin receptor substrate 1 (IRS1) and signal transmiss
27 nsulin resistance by increase in Ser(P)(307)-insulin receptor substrate 1 (IRS1) and subsequent decli
28                           At 32 weeks, lower insulin receptor substrate 1 (IRS1) at S636/639 and Akt
29 ase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307.
30 based gene expression profiling we found the insulin receptor substrate 1 (IRS1) gene as one of the m
31               Common genetic variants in the insulin receptor substrate 1 (IRS1) gene have been recen
32 lele of rs2943641 near the gene encoding for insulin receptor substrate 1 (IRS1) has been associated
33                             Mechanistically, insulin receptor substrate 1 (Irs1) is a direct target o
34                                              Insulin receptor substrate 1 (IRS1) is a key mediator of
35 e reverse-phase protein array, we found that insulin receptor substrate 1 (IRS1) is the most highly u
36 ion against insulin resistance by increasing insulin receptor substrate 1 (IRS1) levels.
37  kinase A (PKA)-dependent phosphorylation of insulin receptor substrate 1 (IRS1) on tyrosine residues
38  known node of PI3K inhibition and decreased insulin receptor substrate 1 (IRS1) protein levels.
39 SHH-treated CGNPs showed increased levels of insulin receptor substrate 1 (IRS1) protein, which was a
40  that has been shown to specifically degrade insulin receptor substrate 1 (IRS1) protein.
41 dent receptor autophosphorylation as well as insulin receptor substrate 1 (IRS1) tyrosine phosphoryla
42                                              Insulin receptor substrate 1 (IRS1) was overexpressed in
43 ndent proteolysis of the CRL7 target protein insulin receptor substrate 1 (IRS1), a component of the
44  insulin-induced tyrosine phosphorylation of insulin receptor substrate 1 (IRS1), activation of prote
45 o trigger multisite seryl phosphorylation of insulin receptor substrate 1 (IRS1), leading to its ubiq
46 LKB1 deletion markedly reduced the levels of insulin receptor substrate 1 (IRS1), peroxisome prolifer
47  PI3K; thus, we examined the requirement for insulin receptor substrate 1 (IRS1), which binds and act
48 h "feedback" phosphorylation of the upstream insulin receptor substrate 1 (IRS1).
49              MiR-487b is predicted to target insulin receptor substrate 1 (IRS1).
50  involves ubiquitin-dependent degradation of insulin receptor substrate 1 (IRS1).
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).
60             The insulin-like growth factor I/insulin receptor substrate 1 axis controls, in a nonredu
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
68 s reduced, whereas serine phosphorylation of insulin receptor substrate 1 was elevated.
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
74                We showed that MEMO1 binds to insulin receptor substrate 1, activates the downstream P
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
82 stance through inhibitory phosphorylation of insulin receptor substrate 1.
83 e a requirement of Rab5 in presenting p85 to insulin receptor substrate 1.
84 r and Akt as well as decreased expression of insulin receptor substrate 1.
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
87 cing a negative feedback signal that targets insulin receptor substrates 1 and 2 (IRS1 and -2).
88 stance is a hallmark of type 2 diabetes, and insulin receptor substrates 1 and 2 (IRS1 and IRS2) are
89                                              Insulin receptor substrates 1 and 2 (IRS1/2) mediate mit
90 insulin signaling through phosphorylation of insulin-receptor substrates 1 and 2 at sites that interf
91        Insulin-stimulated phosphorylation of insulin receptor substrate-1 (IRS-1) and -2, and Akt was
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
96                                              Insulin receptor substrate-1 (IRS-1) and IRS-2 are known
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.
100                    Serine phosphorylation of insulin receptor substrate-1 (IRS-1) can regulate tyrosi
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
103                                          The insulin receptor substrate-1 (IRS-1) is a docking protei
104                                              Insulin receptor substrate-1 (IRS-1) is a signaling adap
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
107                                              Insulin receptor substrate-1 (IRS-1) plays a central rol
108                    Our studies revealed that insulin receptor substrate-1 (IRS-1) protein levels decr
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
111                     In fact, Ad-36 decreased 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
113                These effects are mediated by insulin receptor substrate-1 (IRS-1) via the mitogen-act
114 phoinositide-3 kinase (PI3K) associated with insulin receptor substrate-1 (IRS-1) was attenuated (P <
115                                          The insulin receptor substrate-1 (IRS-1), a docking protein
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
120                        The signaling protein insulin receptor substrate-1 (IRS-1), shown here to be a
121 -high cells, and this enhanced expression of insulin receptor substrate-1 (IRS-1), the principle intr
122                   BT-20 cells do not express insulin receptor substrate-1 (IRS-1), which is known to
123 rtment within tumor cells, where it degraded insulin receptor substrate-1 (IRS-1).
124 ation and degradation of the adaptor protein insulin receptor substrate-1 (IRS-1).
125 ns increases Ser(312) phosphorylation of the insulin receptor substrate-1 (IRS-1).
126 ieving S6K1-dependent negative regulation of insulin receptor substrate-1 (IRS-1).
127 olling ROCK-dependent phosphorylation of the insulin receptor substrate-1 (IRS-1).
128 o regulate insulin signaling at the level of insulin receptor substrate-1 (IRS-1).
129 f key insulin signalling proteins, including insulin receptor substrate-1 (IRS-1).
130 ced phosphorylation of insulin receptor (IR)/insulin receptor substrate-1 (IRS-1)/Akt pathway in the
131               Activation of the insulin (IN)/insulin receptor substrate-1 (IRS-1)/mitogen-associated
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
135                            The gene encoding insulin receptor substrate-1 (IRS1) represents a strong
136            Female mice haploinsufficient for insulin receptor substrate-1 (IRS1-het) are hyperinsulin
137 n turn affects serine 612 phosphorylation of insulin receptor substrate-1 (p612 IRS-1).
138            fADN decreased phosphorylation of insulin receptor substrate-1 (Tyr-608), Akt (Thr-308 and
139 and phosphoinositide 3-kinase decreased, and insulin receptor substrate-1 307 phosphorylation increas
140 timulate glucose transport and phosphorylate Insulin receptor substrate-1 and Akt.
141   Absence of LAR enhanced phosphorylation of insulin receptor substrate-1 and insulin receptor substr
142           In adipose, endotoxemia suppressed insulin receptor substrate-1 and markedly induced suppre
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
146                              This identifies insulin receptor substrate-1 as a novel nonreceptor targ
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
153 , glycogen synthase, and protein kinase B or insulin receptor substrate-1 level was unchanged.
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
158                      We also found increased insulin receptor substrate-1 Ser(636) phosphorylation in
159 significant increases in glucose metabolism, insulin receptor substrate-1, and Akt activity in muscle
160            Skeletal muscle insulin receptor, insulin receptor substrate-1, and Akt contents were unch
161 insulin-signaling pathway (insulin receptor, insulin receptor substrate-1, and Akt).
162 and down-regulation of the insulin receptor, insulin receptor substrate-1, and GLUT4.
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
167  Akt, FoxO1, and c-Src, but did not activate insulin receptor substrate-1-like insulin.
168 TNF-alpha-mediated serine phosphorylation of insulin receptor substrate-1.
169  prevailing model of S6K1 phosphorylation of insulin receptor substrate-1.
170  including sites on the insulin receptor and insulin receptor substrate-1.
171 f the mTOR complex 1-dependent regulation of insulin receptor substrate-1.
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
175 cking either insulin receptors (betaIRKO) or insulin receptor substrate 2 (betaIRS2KO).
176                    Appropriate regulation of insulin receptor substrate 2 (IRS-2) expression in pancr
177                                              Insulin receptor substrate 2 (IRS-2) plays a critical ro
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
184                                          The insulin receptor substrate 2 (Irs2) branch of the insuli
185 a/cAMP mediates these actions by stimulating insulin receptor substrate 2 (IRS2) expression.
186 s, proliferation, and survival by increasing insulin receptor substrate 2 (IRS2) levels and identify
187                                              Insulin receptor substrate 2 (IRS2) suppression induced
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
195                                              Insulin receptor substrate-2 (IRS-2) belongs to the IRS
196 related with tyrosine phosphorylation of the insulin receptor substrate-2 (IRS-2) in macrophages.
197                                              Insulin receptor substrate-2 (IRS-2) plays a critical ro
198                                              Insulin receptor substrate-2 (IRS-2) plays an essential
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
203                                              Insulin receptor substrate-2 (Irs2) is a critical mediat
204            Here, we show that, in mice, less insulin receptor substrate-2 (Irs2) signaling throughout
205                                  We identify insulin receptor substrate-2 (Irs2), a known cAMP-respon
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
213            Using mass spectrometric analysis insulin receptor substrate 4 (IRS-4) has been identified
214                  One interacting protein was insulin receptor substrate 4 (IRS-4), a member of the IR
215 hyperinsulinemic-euglycemic clamp and muscle insulin receptor substrate and Akt phosphorylation demon
216 thways governing glucose metabolism, such as insulin receptor substrate and Akt substrate.
217       PKR also directly targets and modifies insulin receptor substrate and hence integrates nutrient
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
220           TNF-alpha inhibits the function of insulin receptor substrates and decreases the expression
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
223                                              Insulin receptor substrates, including Irs1 and Irs2, in
224 n the level of serine phosphorylation of the insulin receptor substrate IRS-1.
225                       These foci contain the insulin receptor substrate (IRS) 1 adaptor molecule, and
226 easured the life span of mice lacking either insulin receptor substrate (IRS) 1 or 2, the major intra
227                                              Insulin receptor substrate (IRS) 2 as intermediate docki
228 IS/TOR network, including the critical nodes insulin receptor substrate (IRS) and phosphatidylinosito
229                                          The insulin receptor substrate (IRS) proteins are cytoplasmi
230                                          The insulin receptor substrate (IRS) proteins are cytoplasmi
231 ammatory cytokines induce phosphorylation of insulin receptor substrate (IRS) proteins at Ser sites t
232                                          The insulin receptor substrate (IRS) proteins represent a cr
233                                          The insulin receptor substrate (IRS) proteins serve as essen
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
236           The mRNA transcript levels of AAH, insulin receptor substrate (IRS), insulin and insulin-li
237                        Mice with deletion of insulin receptor substrate (IRS)-1 (IRS-1 knockout [KO]
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
240                                      Hepatic insulin receptor substrate (IRS)-1 and IRS-2 expression
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
246                               Suppression of insulin receptor substrate (IRS)-1 and tuberous sclerosi
247                      Research has focused on insulin receptor substrate (IRS)-1 as a locus for insuli
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
255                         Insulin receptor and insulin receptor substrate (IRS)-1 serine hyperphosphory
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
260                           Phosphorylation of insulin receptor substrate (IRS)-1/2 by IGF-I receptor t
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
267             Furthermore, we also showed that insulin receptor substrate (IRS)-2, but not IRS-1, is in
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
270           Postreceptor signaling through the insulin receptor substrate (IRS)/PI3-K/Akt pathway was e
271 ikely caused by, direct dephosphorylation of insulin receptor substrate (IRS)1/2 in the liver, accomp
272                                     We found insulin receptor substrate (IRS)2 and enhanced-activated
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
276       When phosphorylated by mTORC1/S6K, the insulin receptor substrate (IRS-1) is targeted for ubiqu
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
279                                              Insulin receptor substrates (Irs-proteins) integrate sig
280 ut displayed severely blunted signalling via insulin-receptor substrate (IRS) proteins, key mediators
281 d phosphorylation of IGF signaling molecules insulin-receptor substrate (IRS)-1 and IRS-2.
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
284  tyrosine phosphorylation of adapter protein insulin receptor substrate (IRS1).
285  This is the result of downregulation of the insulin receptor substrates, IRS1 and IRS2, which become
286                                              Insulin receptor substrates (IRSs) are signaling adaptor
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.
289 ovel PDZ1 binding partner, the I-BAR protein insulin receptor substrate p53 (IRSp53).
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
294                                   The 53 kDa insulin receptor substrate protein (IRSp53) is highly en
295 ess at least two Tiam1-interacting proteins, insulin receptor substrate protein 53 kDa (IRSp53) and s
296                          DOK1 is a member of insulin receptor substrate protein family that binds bet
297 of the insulin signaling pathways engaged by insulin receptor substrate proteins.
298 ting Tyr-325 was not required for the robust insulin receptor substrate response.
299  results from differential downregulation of insulin receptor substrates that control phosphatidylino
300 sed muscle insulin signaling (phosphorylated insulin receptor substrate(Tyr) and Akt(Ser473) levels)

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