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1 g proteins, insulin receptor substrate 1 and insulin receptor substrate 2.
2 th Y497F were not capable of phosphorylating insulin receptor substrate 2.
3 binding to insulin receptor substrate-1 and insulin receptor substrate-2, activation of PI3K and pro
4 results in enhanced IR signaling through the insulin receptor substrate 2-AKT pathway in beta-cells a
7 alues, whereas only VV-TPN increased hepatic insulin receptor substrate 2 and maintained normal hepat
9 , no significant tyrosine phosphorylation of insulin receptor substrate-2 and modulation of the immed
10 IL-10 increased tyrosyl phosphorylation of insulin receptor substrate-2 and stimulated the enzymati
11 ted tyrosine phosphorylation of JAK kinases, insulin receptor substrate-2, and signal transducer and
12 uced cell growth, activation of JAK kinases, insulin receptor substrate-2, and STAT3 and expression o
13 n key insulin-signaling molecules, including insulin receptor substrate-2, and substrate metabolism t
14 ximately 40% reduction in insulin-stimulated insulin receptor substrate-2-associated phosphatidylinos
15 ciated with defects in insulin activation of insulin receptor substrate-2-associated phosphatidylinos
17 cy appeared necessary for phosphorylation of insulin receptor substrate-2 but not for IGFR1 activatio
20 kinase 1, insulin receptor substrate 1, and insulin receptor substrate 2, factors with molecular mas
22 es IGF-I-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2) and inhibits IRS-2-
25 oved insulin-stimulated insulin receptor and insulin receptor substrate 2 (IRS-2) phosphorylation, IR
27 ubsequent 52% decrease in insulin-stimulated insulin receptor substrate 2 (IRS-2) tyrosine phosphoryl
29 cAMP response element-binding protein (CREB)-insulin receptor substrate 2 (Irs-2), and increased beta
30 the brain, targets insulin receptor (INSR), insulin receptor substrate 2 (IRS-2), and insulin-degrad
31 that promotes beta-cell growth and survival, insulin receptor substrate 2 (IRS-2), is a member of a f
32 insulin-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2), whereas it had min
35 related with tyrosine phosphorylation of the insulin receptor substrate-2 (IRS-2) in macrophages.
43 to abused drugs decreases the expression of insulin receptor substrate-2 (IRS-2; a protein involved
44 GM-CSF) induced tyrosine phosphorylation of insulin-receptor substrate-2 (IRS-2) and its association
45 ptor (Igf1r(+/-)) are bred with mice lacking insulin receptor substrate 2 (Irs2(-/-)), the resulting
46 teins involved in insulin signaling, such as insulin receptor substrate 2 (IRS2) and glucose transpor
48 3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, there
49 component of all types of diabetes, and the insulin receptor substrate 2 (IRS2) branch of signaling
52 Here we show that a conditional knockout of insulin receptor substrate 2 (Irs2) in mouse pancreas be
54 s, proliferation, and survival by increasing insulin receptor substrate 2 (IRS2) levels and identify
56 s is sufficient to enhance the expression of insulin receptor substrate 2 (IRS2) to levels observed i
57 MR-409 induces Akt signaling by induction of insulin receptor substrate 2 (IRS2), a master regulator
58 2)-associated binding proteins 1-3 (GAB1-3), insulin receptor substrate 2 (IRS2), docking protein 1 (
59 mice lacking insulin signaling intermediate insulin receptor substrate 2 (IRS2), we confirmed that h
60 The study also provides strong evidence that insulin receptor substrate 2 (Irs2), which is known to h
61 ronic morphine-induced downregulation of the insulin receptor substrate 2 (IRS2)-thymoma viral proto-
62 of sarcomas and found a marked induction of insulin receptor substrate-2 (IRS2) and phosphorylated A
65 hat mice heterozygous for a null mutation in insulin receptor substrate-2 (Irs2) display a 17% increa
66 3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstr
70 ing through direct and indirect induction of insulin receptor substrate-2 (Irs2), an essential insuli
71 s (week 15); liver and adipose AhR and IRS2 (insulin receptor substrate 2) mRNA abundance, and PCB-77
72 ysis occurs normally in B cells deficient in insulin receptor substrate-2 or the p85alpha subunit of
73 d the downstream signaling pathway involving insulin receptor substrate 2, phosphatidylinositol 3'-ki
75 s with inhibition of NF-kappaB showed normal insulin receptor substrate-2 phosphorylation and only a
77 vity is totally due to IL-10 stimulating the insulin receptor substrate-2/PI 3-kinase/Akt pathway, wh
80 eas insulin receptor autophosphorylation and insulin receptor substrate 2 tyrosine phosphorylation we
81 pression of glucose transporters 1 and 4 and insulin receptor substrate 2 was increased and that of p
82 sducer and activator of transcription 6, and insulin receptor substrate 2 was strikingly but transien
84 nsulin-dependent tyrosine phosphorylation of insulin receptor substrate-2 was enhanced in the p85beta
85 The hepatic mRNA level of the HIF-2 target insulin receptor substrate-2 was higher, whereas that of
86 ic screen of HD, we found that activation of insulin receptor substrate-2, which mediates the signali
87 lts in decreased tyrosine phosphorylation of insulin receptor substrate-2 with impeded insulin signal