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1 significant numbers of cells expressing the IGF receptor.
2 mediated through interaction with the type 1 IGF receptor.
3 nity similar to that of IGF-I for the type I IGF receptor.
4 n NIH 3T3 cells over-expressing human type-I IGF receptor.
5 , which control their access to cell-surface IGF receptors.
6 hich allows IGF-I to better equilibrate with IGF receptors.
7 n experiments revealed galectin-3 binding to IGF-receptor 1 (R1), thus suggesting that interaction of
8 s to IGF-2 (18% cell death), antibody to the IGF receptor (45% cell death), and IGF-1 antisense oligo
9 ve studied the mechanism by which endogenous IGF receptors activate the ERK1/2 mitogen-activated prot
14 is rapidly internalized after binding to the IGF receptor and is rapidly catabolized with release of
15 fibroblasts also accumulate acidic vesicles, IGF receptor and transferrin, indicating that dysferlin
16 on is mediated by high affinity cell surface IGF receptors and modulated by a family of secreted IGF
17 RS), insulin and insulin-like growth factor (IGF) receptors and polypeptides, Notch, Jagged, and HES
18 nd IGF-2, an antibody that blocks the type 1 IGF receptor, and antisense oligonucleotides to inhibit
19 he actions of IGF-I at a point distal to the IGF receptor, and this was not due to IL-1beta-induced c
22 ion system inhibited DNA synthesis in an IGF-IGF receptor axis-independent fashion and resulted in th
24 anti-IGF-II, anti-insulin receptor, or anti-IGF receptor blocking antibodies caused a significant de
25 t monkeys in the presence and absence of the IGF receptor blocking antibody and ceramide to induce ce
28 2 gene, or conditional disruption of the two IGF receptor genes Igf1r and Insr together in the myocar
31 ndent tyrosine phosphorylation of the type I IGF receptor (IGF-IR) and extracellular signal-regulated
32 rated that SHPS-1 was a substrate for type I IGF receptor (IGF-IR) and that IRS-1 competitively inhib
33 ast cancer cells to inhibitors of the type I IGF receptor (IGF-IR) in a manner reversed by the reacti
34 (IGF-I) to induce phosphorylation of type I IGF receptor (IGF-IR), insulin receptor substrate 1, pho
36 1, including enhanced phosphorylation of the IGF receptor (IGF-R) and insulin receptor substrate as w
42 ment to evaluate the potential of the type 1 IGF receptor (Igf1r) for targeted anticancer therapy in
43 (IGF-I and IGF-II) and their cognate type 1 IGF receptor (IGF1R) have demonstrated that this signali
44 lonal antibodies directed against the type I IGF receptor (IGF1R) in combination with estrogen recept
48 king GPC3 and also IGF2, IGF1, or the type 1 IGF receptor (IGF1R) provided conclusive genetic evidenc
50 s by disrupting the gene encoding the type 1 IGF receptor (IGF1R) specifically in the mouse brain by
51 hile IGF signaling is mediated by the type 1 IGF receptor (IGF1R), the type 2 receptor (IGF2R/CI-MPR)
53 le of the type I insulin-like growth factor (IGF) receptor (IGF1R) in cancer metastasis we inhibited
55 for both IGF-I and IGF-II, as well as type-2 IGF receptor (IGF2R) mRNA was not found to be altered du
57 In this study, we examined the role of the IGF receptor (IGFR) and the importance of IGFR glycosyla
59 hat neutralization of IGF action by a type I IGF receptor (IGFR1) blocking antibody or neutralization
60 signaling pathways downstream of the type I IGF receptor in a subset of malignant pleural mesothelio
63 itated the autophosphorylation of the type 1 IGF receptor, increased class IA phosphatidylinositol 3'
67 daf-2, an insulin/insulinlike growth factor (IGF) receptor (INR) homolog gene, were profoundly Hyp.
69 results demonstrate that IGF-1 activates the IGF receptor/IRS/PI3K/PKB pathway, and that PI3Kalpha is
71 .3-3.9 nM) and no biological activity at the IGF receptors (Ki = >10,000 nM) increased the levels of
73 pathway independent of either p53 or the IGF.IGF receptor-mediated cell survival pathway and that IGF
74 r (IGFR) and is essential for activating the IGF receptor-mediated intracellular signalling pathway.
76 ected insulin, IGF-II, insulin receptor, and IGF receptor mRNAs in both the neural tube and the somit
79 bound IGFBP-3 allows IGF-I release to type I IGF receptors of stromal cells migrating into the fibrin
82 of the patients expressed activated insulin/IGF receptors on tumor cells, and this positively correl
83 of insulin-like signaling via DAF-2 insulin/IGF receptor or its intramuscular effector PtdIns-3-kina
84 rent from those resulting from deficiency of Igf receptor or ligand in zebrafish, suggesting a functi
87 e to nutrition, and we show that the insulin/IGF receptor pathway is necessary for neuroblasts to exi
88 el with the glp-1 (Notch) and daf-2 (insulin-IGF receptor) pathways, and does not share the same gene
89 ing the survival effect of IGF-I we examined IGF receptor phosphorylation and Akt phosphorylation and
91 The IGF pathway, acting through the type 1 IGF-receptor, repressed apoptosis of lung fibroblasts bu
92 of DOG1 in GIST involving modulation of IGF/IGF receptor signaling in the tumor microenvironment thr
93 at STC2 efficiently inhibits PAPP-A-mediated IGF receptor signaling in vitro and that transgenic mice
96 cluding Irs1 and Irs2, integrate insulin and IGF receptor signals with heterologous pathways to coord
97 ibody (alphaIR3) directed against the type 1 IGF receptor significantly attenuated the ability of IGF
99 f2r gene on chromsome 17 encoding the type 2 IGF receptor that is involved in degradation of excess I
100 ect of antisense insulin-like growth factor (IGF) receptor transcripts on the proliferation and tumor
101 factor in several tumor types by binding to IGF receptor type 1 (IGF-1R) and/or the insulin receptor
102 .05) decrease in insulin-like growth factor (IGF) receptor type I beta and an approximately 13-fold (
103 Cell death from inhibition of the type 1 IGF receptor was associated with an increase in caspase
104 were those from young adult monkeys when the IGF receptor was blocked and cell death was further stim
105 afficking of the insulin-like growth factor (IGF) receptor, where the receptor is shuttled to LAMP2-p
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