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1 PDGFR-beta has become an attractive target for the treat
2 PDGFR-beta inhibition selectively eliminates morphine to
3 PDGFR-beta inhibitors are widely used and well tolerated
4 PDGFR-beta is necessary for flow-induced neointimal form
5 PDGFR-beta promotes growth of mesenchymal cells, includi
6 of both these single agents against VEGFR-2, PDGFR-beta, and hTS is better than or close to standards
8 sduction, we have generated mice that bear a PDGFR-beta that can no longer activate PI3kinase or PLCg
9 DGFR-alpha; 10 mg/kg; n=5) or PDGFR-beta (Ab-PDGFR-beta; 10 mg/kg; n=6) by pulsed intravenous adminis
10 w/high flow) was significantly reduced in Ab-PDGFR-beta (1.2+/-0.2, P<0.01) but not in Ab-PDGFR-alpha
12 l rapidly after day 7 to 0, whereas serum Ab-PDGFR-beta concentrations were maintained at the target
13 revealed close association between activated PDGFR-beta and LRP, suggesting that LRP functions as a c
16 s the benefits of targeted therapies against PDGFR-beta in aggressive life-threatening familial forms
17 n Ang-2 null mutants, alpha SMA, desmin, and PDGFR beta prominently immunolocalized in cortical perit
18 type I cytokine receptors (EGFR, IL-1R, and PDGFR-beta), type II cytokines (bFGF, LIF, and TGF-beta
26 ligand-mediated activation of IGF1R-beta and PDGFR-beta are reversed by co-treatment of the cells wit
27 d-independent manner, whereas IGF1R-beta and PDGFR-beta require ligand interaction for activation.
28 bserved in areas of F4/80(+) macrophages and PDGFR-beta(+) and transgelin(+) fibroblasts, all of whic
29 g using cells established from wild-type and PDGFR-beta -/- metanephric blastemas at 11.5 days post-c
31 f reagents (an anti-VEGF aptamer and an anti-PDGFR-beta antibody) to inhibit both the VEGF-A and PDGF
32 were injected daily with a neutralizing anti-PDGFR-beta antibody (APB5), an anti-PDGFR-alpha antibody
33 y of 17 (JNJ-10198409), a compound with anti-PDGFR-beta kinase activity (IC(50)=0.0042 microM) and po
35 tic chimeras reconstituted with PDGF-B(-/-), PDGFR beta(-/-), or wild-type fetal liver cells show com
40 latelet-derived growth factor receptor beta (PDGFR beta) and PDGFR alpha, but not insulin-like growth
42 latelet-derived growth factor receptor beta (PDGFR beta), and desmin-expressing cells were not promin
43 latelet-derived growth factor receptor beta (PDGFR-beta) expression in malignancies, we have cloned a
44 latelet-derived growth factor receptor beta (PDGFR-beta) has been associated with cancers and vascula
45 latelet-derived growth-factor receptor beta (PDGFR-beta) tyrosine kinase is required for proper forma
46 nds at Tyr-1009 in human PDGF receptor beta (PDGFR-beta) which is different from Nckalpha's binding s
48 latelet-derived growth factor receptor-beta (PDGFR-beta) for antiangiogenic effects and also inhibit
49 latelet-derived growth factor receptor-beta (PDGFR-beta) leads to tyrosine phosphorylation of the cyt
52 receptor 2 (VEGFR2) and PDGF receptor-beta (PDGFR-beta) were blunted in diabetic Prkcd(+/+) mice but
53 ed that LOX oxidizes the PDGF receptor-beta (PDGFR-beta), leading to amplified downstream signaling.
55 latelet-derived growth factor receptor-beta (PDGFR-beta)-mediated signaling plays a key role in morph
56 or tyrosine kinases (RTKs), i.e. IGF1R-beta, PDGFR-beta, EGFR and c-MET, in colon, prostate, and brea
59 us, myointimal proliferation depends on both PDGFR-beta overexpression and its activation by PDGF-BB.
61 These results demonstrate that cardiomyocyte PDGFR-beta is a regulator of the compensatory cardiac re
62 echanistically, we showed that cardiomyocyte PDGFR-beta signaling plays a vital role in stress-induce
63 ifically, we demonstrated that cardiomyocyte PDGFR-beta was an essential upstream regulator of the st
64 ed PDGF-dependent cellular function, certain PDGFR-beta-induced signal cascades are not essential for
65 plasmic domain mutants of the chimeric M-CSF/PDGFR-beta, we confirmed that the kinase domain of PDGFR
66 skin is impaired, correlating with defective PDGFR-beta and transforming growth factor-beta (TGF-beta
69 EGF, TGF-alpha upregulated additional EGFR, PDGFR-beta, bFGF, and TGF-beta 1, suggesting that althou
70 me of the alpha SMA-positive cells expressed PDGFR beta, desmin, and neural/glial cell 2 (NG2), consi
72 s mitogenic for mesenchymal cells expressing PDGFR-beta, and PI3-K is an important regulator of PDGF-
74 ol/L) being more than 450-fold selective for PDGFR-beta versus other angiogenic receptors (e.g., vasc
76 telomestatin significantly reduced the human PDGFR-beta basal promoter activity relative to the contr
77 clease hypersensitivity element of the human PDGFR-beta gene promoter have been found to inhibit PDGF
78 d the first functional promoter of the human PDGFR-beta gene, which has been confirmed by luciferase
80 region (positions -165 to -139) of the human PDGFR-beta promoter is crucial for basal promoter activi
84 orphogenesis reminiscent of that observed in PDGFR-beta-/- mice with significantly reduced immunostai
85 indings indicate p.Arg561Cys substitution in PDGFR-beta as a cause of the dominant form of this disea
86 ndent signal transduction pathway, including PDGFR-beta, SHP2, AKT1, and ERK1/ERK2 (p44/42 MAPK), tur
91 ic reporter mouse, we showed that inhibiting PDGFR-beta activation restricted the distribution of col
98 and extracellular ligand binding domains of PDGFR beta (exons 2-23) and c-kit (exons 1-21) in 6 pati
101 nd PDGF-BB-stimulated autophosphorylation of PDGFR-beta in cells (IC(50) = 1 nmol/L) being more than
103 beta, we confirmed that the kinase domain of PDGFR-beta is absolutely required for LRP tyrosine phosp
104 lmost completely abolished the expression of PDGFR-beta protein in the intima and media of injured ca
105 hese observations suggest that inhibition of PDGFR-beta might improve delivery of a concurrently admi
108 ukemic cells expressed much higher levels of PDGFR-beta transcripts than purified normal CD8(+) T cel
109 r metastatic potential, and higher levels of PDGFR-beta were expressed on cells with lower metastatic
110 These models include an ex vivo measure of PDGFR-beta phosphorylation in glioblastoma tumors, a spo
111 73,451 and to understand the pharmacology of PDGFR-beta inhibition and the effect on tumor growth.
112 nd preserving stemness-related properties of PDGFR-beta(+) MSCs, including the ability to repopulate
113 This study highlights the significance of PDGFR-beta signaling for the recruitment, proliferation,
116 dy demonstrates that hematopoietic PDGF-B or PDGFR beta expression is not required for hematopoiesis
118 GFR-alpha (Ab-PDGFR-alpha; 10 mg/kg; n=5) or PDGFR-beta (Ab-PDGFR-beta; 10 mg/kg; n=6) by pulsed intr
120 thesis that inhibiting either PDGFR-alpha or PDGFR-beta with a specific mouse/human chimeric antibody
121 one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors, and most tumors
122 sults indicate that RGS5 exerts control over PDGFR-beta and GPCR-mediated signaling pathways active d
124 ding of PDGF-BB by cells containing oxidized PDGFR-beta was diminished by approximately 2-fold when c
125 te markers in carcinoma cells, in particular PDGFR-beta and N-cadherin, which enabled EMT cells to be
126 Perivascular cells expressing phosphorylated PDGFR-beta were identified in the infarct after 7 days o
127 le formation, including podocalyxin (Podxl), PDGFR-beta, and a follistatin-domain-encoding gene Flst1
128 e shown that PDGF-D and its cognate receptor PDGFR-beta are expressed in prostate tumor tissues, sugg
129 essed by endothelial cells, and its receptor PDGFR-beta, expressed by pericytes, plays a central role
130 owth factor (PDGF)-B and PDGF beta-receptor (PDGFR beta) deficiency in mice is embryonic lethal and r
131 latelet-derived growth factor beta-receptor (PDGFR-beta) kinase- and PDGF-BB-stimulated autophosphory
132 of platelet-derived growth factor receptor (PDGFR-beta) was specifically downregulated in mutant fib
134 ast growth factor receptors, VEGF receptors, PDGFR-beta, and c-KIT, as second-line therapy both in pa
135 otides to reduce PDGF-beta receptor subunit (PDGFR-beta) expression and the contribution of PDGFR-bet
137 studies of rat embryonic kidneys reveal that PDGFR beta localizes to undifferentiated metanephric mes
138 ed for LRP tyrosine phosphorylation but that PDGFR-beta-mediated activation of phosphatidylinositol 3
139 As described herein, we have found that PDGFR-beta expression and activation increase dramatical
142 y the cellular compartment where LRP and the PDGFR-beta may interact, we employed immunofluorescence
151 or in which the ligand binding domain of the PDGFR-beta was replaced with that from the macrophage co
154 e oligonucleotide sequences complementary to PDGFR-beta mRNA almost completely abolished the expressi
156 ly selective PDGFR inhibitor, inhibits tumor PDGFR-beta phosphorylation, selectively inhibits PDGF-BB
157 nt on PI3-K activation were determined using PDGFR-beta -/- cells made to express "add-back" mutant P
159 ls initially enter the thymus at E13.5, with PDGFR-beta(+) mesenchymal cells following at E14.5.
160 a cell-autonomous manner, acting in cis with PDGFR-beta and TGF-beta receptors during induction/polar
161 und that wild-type LRP6 forms a complex with PDGFR-beta and enhances its lysosomal degradation, funct
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