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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
7                                   Both E14.5 PDGFR-beta- and platelet-derived growth factor (PDGF)-B-
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
11 0.01) compared with either the control or Ab-PDGFR-beta treated groups.
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
14                                 In addition, PDGFR-beta inhibition in vivo was accompanied by abnorma
15                                 In addition, PDGFR-beta signaling mediates coating of developing vess
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
19               Higher expression of p-AKT and PDGFR-beta were associated with shorter PFS, and higher
20 iments confirmed the role of PDGFR-alpha and PDGFR-beta as receptors for AAV-5.
21 atinib mesylate blocked both PDGFR-alpha and PDGFR-beta in vivo.
22  decreased the expression of PDGFR-alpha and PDGFR-beta throughout differentiation.
23 actions with PDGF receptor (PDGFR)-alpha and PDGFR-beta.
24                 The PDGF-B, PDGFR-alpha, and PDGFR-beta mRNA expression was induced in reperfused mou
25 nd signaling of PDGF-receptor (R)-alpha- and PDGFR-beta-chains.
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
30                 The inhibition of VEGFR2 and PDGFR-beta activity was associated with increased SHP-1
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
34 zing specific cell surface proteins, such as PDGFR-beta.
35 tic chimeras reconstituted with PDGF-B(-/-), PDGFR beta(-/-), or wild-type fetal liver cells show com
36                         Activation of PDGF-B/PDGFR-beta is also involved in recruitment of mural cell
37       Pharmacologic inhibition of the PDGF-B/PDGFR-beta signaling axis disrupted the association of m
38 fusion, indicating activation of the PDGF-BB/PDGFR-beta pathway.
39 e regenerative potential of MSCs via PDGF-BB/PDGFR-beta signaling.
40 latelet-derived growth factor receptor beta (PDGFR beta) and PDGFR alpha, but not insulin-like growth
41 actor (PDGF) B-chain and PDGF receptor beta (PDGFR beta) are essential for glomerulogenesis.
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
47  and colocalization with PDGF receptor beta (PDGFR-beta).
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
50 latelet-derived growth factor receptor-beta (PDGFR-beta) signaling during MC recruitment.
51 latelet-derived growth factor receptor-beta (PDGFR-beta) subunit after vascular injury.
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.
54  proteins, including the PDGF receptor-beta (PDGFR-beta), to affect PDGF-BB-induced chemotaxis.
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
57                                     Blocking PDGFR-beta signaling did not prevent the differentiation
58                                         Both PDGFR-beta- and PDGFR-alpha-mediated pathways promote co
59 us, myointimal proliferation depends on both PDGFR-beta overexpression and its activation by PDGF-BB.
60          Pericyte coverage was determined by PDGFR-beta and alpha-SMA staining.
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
67      Northern blot analysis failed to detect PDGFR-beta mRNA in mutant cells.
68 8 and M-CSF expression, but it downregulated PDGFR-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
71 2.5% of medial smooth muscle cells expressed PDGFR-beta.
72 s mitogenic for mesenchymal cells expressing PDGFR-beta, and PI3-K is an important regulator of PDGF-
73 othelial HS appears sufficient to facilitate PDGFR-beta activation in trans.
74 ol/L) being more than 450-fold selective for PDGFR-beta versus other angiogenic receptors (e.g., vasc
75          These cells also express functional PDGFR beta, as demonstrated by autophosphorylation of th
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
79 pecific G-quadruplex structures in the human PDGFR-beta promoter can modulate its transcription.
80 region (positions -165 to -139) of the human PDGFR-beta promoter is crucial for basal promoter activi
81 fferent G-quadruplex structures of the human PDGFR-beta promoter.
82                            Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.
83 h the pericyte marker (immunohistochemistry: PDGFR-beta) and CK19.
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
87 ed by significant upregulation and increased PDGFR-beta signaling.
88        However, the importance of individual PDGFR-beta signal transduction pathways in vivo is not k
89              PDGF-BB with nanofibers induced PDGFR-beta and Akt phosphorylation in cardiomyocytes in
90 eta gene promoter have been found to inhibit PDGFR-beta transcriptional activity.
91 ic reporter mouse, we showed that inhibiting PDGFR-beta activation restricted the distribution of col
92                  In this study, we localized PDGFR beta in the developing rat kidney and explored the
93                       In all animals, medial PDGFR-beta expression doubled 2 weeks after endothelial
94 target this secondary structure and modulate PDGFR-beta gene expression.
95  -/- cells made to express "add-back" mutant PDGFR-beta capable of binding PI3-K.
96 the mutant mice that suggest that the mutant PDGFR-beta operates at suboptimal levels.
97  mutations in the genes SMARCA4, EPHA3, MYB, PDGFR-beta, and PIK3CA.
98  and extracellular ligand binding domains of PDGFR beta (exons 2-23) and c-kit (exons 1-21) in 6 pati
99             We have mapped Y740 as a site of PDGFR beta that is involved in the association with PSM.
100       RasGAP, that responds to activation of PDGFR-beta but not PDGFR-alpha, was not phosphorylated o
101 nd PDGF-BB-stimulated autophosphorylation of PDGFR-beta in cells (IC(50) = 1 nmol/L) being more than
102 GFR-beta) expression and the contribution of PDGFR-beta in neointimal formation.
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
106                                Inhibition of PDGFR-beta phosphorylation in tumors correlates with pla
107 ating TPH1 down-regulation via inhibition of PDGFR-beta signaling.
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,
114 PDGF-C(-/-) mice) or even an upregulation of PDGFR-beta and signaling (anti-PDGF-C group).
115 ies that are characterized by either abl- or PDGFR beta- activating mutations.
116 dy demonstrates that hematopoietic PDGF-B or PDGFR beta expression is not required for hematopoiesis
117            Mice deficient in PDGF B-chain or PDGFR beta exhibit an abnormal glomerular phenotype char
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
119 ed by increased expression of PDGFR-alpha or PDGFR-beta in NSCLC cells.
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
123 purified from control SMC contained oxidized PDGFR-beta.
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
133 the platelet-derived growth factor receptor (PDGFR-beta).
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
136                                    Targeting PDGFR-beta may be an effective pharmacological strategy
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
140       Studies in animals have suggested that PDGFR-beta inhibition reduces tumor interstitial fluid p
141                                          The PDGFR-beta blockade resulted in impaired maturation of t
142 y the cellular compartment where LRP and the PDGFR-beta may interact, we employed immunofluorescence
143        The transcription initiation from the PDGFR-beta gene promoter was not significantly changed,
144                             Furthermore, the PDGFR-beta mRNA level in Daoy cells was significantly de
145 ermined the major G-quadruplex formed in the PDGFR-beta promoter.
146         Further, phosphorylated forms of the PDGFR-beta co-immunoprecipitated with LRP following PDGF
147  plays a specific role in the control of the PDGFR-beta expression.
148 thelial cells in vitro via inhibition of the PDGFR-beta pathway.
149                     The novel folding of the PDGFR-beta promoter G-quadruplex emphasizes the robustne
150                     The novel folding of the PDGFR-beta promoter G-quadruplex may be attractive for s
151 or in which the ligand binding domain of the PDGFR-beta was replaced with that from the macrophage co
152                Phosphorylated members of the PDGFR-beta-dependent signal transduction pathway, includ
153  the potent migratory factor PDGF-BB through PDGFR-beta.
154 e oligonucleotide sequences complementary to PDGFR-beta mRNA almost completely abolished the expressi
155                           Binding of PDGF to PDGFR-beta induces autophosphorylation at specific tyros
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
158                      SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed i
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
162 ointimal formation correlated precisely with PDGFR-beta expression in an exponential fashion.

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