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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
8 , no significant tyrosine phosphorylation of insulin receptor substrate-2 and modulation of the immed
9 IL-10 increased tyrosyl phosphorylation of insulin receptor substrate-2 and stimulated the enzymati
10 ted tyrosine phosphorylation of JAK kinases, insulin receptor substrate-2, and signal transducer and
11 uced cell growth, activation of JAK kinases, insulin receptor substrate-2, and STAT3 and expression o
12 n key insulin-signaling molecules, including insulin receptor substrate-2, and substrate metabolism t
13 ximately 40% reduction in insulin-stimulated insulin receptor substrate-2-associated phosphatidylinos
14 ciated with defects in insulin activation of insulin receptor substrate-2-associated phosphatidylinos
16 cy appeared necessary for phosphorylation of insulin receptor substrate-2 but not for IGFR1 activatio
19 kinase 1, insulin receptor substrate 1, and insulin receptor substrate 2, factors with molecular mas
21 es IGF-I-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2) and inhibits IRS-2-
24 oved insulin-stimulated insulin receptor and insulin receptor substrate 2 (IRS-2) phosphorylation, IR
26 ubsequent 52% decrease in insulin-stimulated insulin receptor substrate 2 (IRS-2) tyrosine phosphoryl
28 that promotes beta-cell growth and survival, insulin receptor substrate 2 (IRS-2), is a member of a f
29 insulin-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2), whereas it had min
32 related with tyrosine phosphorylation of the insulin receptor substrate-2 (IRS-2) in macrophages.
40 to abused drugs decreases the expression of insulin receptor substrate-2 (IRS-2; a protein involved
41 GM-CSF) induced tyrosine phosphorylation of insulin-receptor substrate-2 (IRS-2) and its association
42 ptor (Igf1r(+/-)) are bred with mice lacking insulin receptor substrate 2 (Irs2(-/-)), the resulting
43 teins involved in insulin signaling, such as insulin receptor substrate 2 (IRS2) and glucose transpor
45 3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, there
46 component of all types of diabetes, and the insulin receptor substrate 2 (IRS2) branch of signaling
49 Here we show that a conditional knockout of insulin receptor substrate 2 (Irs2) in mouse pancreas be
50 s, proliferation, and survival by increasing insulin receptor substrate 2 (IRS2) levels and identify
52 s is sufficient to enhance the expression of insulin receptor substrate 2 (IRS2) to levels observed i
53 2)-associated binding proteins 1-3 (GAB1-3), insulin receptor substrate 2 (IRS2), docking protein 1 (
54 mice lacking insulin signaling intermediate insulin receptor substrate 2 (IRS2), we confirmed that h
55 The study also provides strong evidence that insulin receptor substrate 2 (Irs2), which is known to h
56 ronic morphine-induced downregulation of the insulin receptor substrate 2 (IRS2)-thymoma viral proto-
57 of sarcomas and found a marked induction of insulin receptor substrate-2 (IRS2) and phosphorylated A
60 hat mice heterozygous for a null mutation in insulin receptor substrate-2 (Irs2) display a 17% increa
61 3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstr
65 ing through direct and indirect induction of insulin receptor substrate-2 (Irs2), an essential insuli
66 ysis occurs normally in B cells deficient in insulin receptor substrate-2 or the p85alpha subunit of
67 d the downstream signaling pathway involving insulin receptor substrate 2, phosphatidylinositol 3'-ki
69 s with inhibition of NF-kappaB showed normal insulin receptor substrate-2 phosphorylation and only a
71 vity is totally due to IL-10 stimulating the insulin receptor substrate-2/PI 3-kinase/Akt pathway, wh
73 eas insulin receptor autophosphorylation and insulin receptor substrate 2 tyrosine phosphorylation we
74 pression of glucose transporters 1 and 4 and insulin receptor substrate 2 was increased and that of p
75 sducer and activator of transcription 6, and insulin receptor substrate 2 was strikingly but transien
77 nsulin-dependent tyrosine phosphorylation of insulin receptor substrate-2 was enhanced in the p85beta
78 The hepatic mRNA level of the HIF-2 target insulin receptor substrate-2 was higher, whereas that of
79 ic screen of HD, we found that activation of insulin receptor substrate-2, which mediates the signali
80 lts in decreased tyrosine phosphorylation of insulin receptor substrate-2 with impeded insulin signal
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