ライフサイエンスコーパス: PDGFR-beta

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 latelet-based growth variable receptor beta (PDGFR-beta), Bcl2, Cathepsine, and MMP-2 gene expression

48 and colocalization with PDGF receptor beta (PDGFR-beta).

49 latelet-derived growth factor receptor-beta (PDGFR-beta) for antiangiogenic effects and also inhibit

50 latelet-derived growth factor receptor-beta (PDGFR-beta) leads to tyrosine phosphorylation of the cyt

51 latelet-derived growth factor receptor-beta (PDGFR-beta) signaling during MC recruitment.

52 latelet-derived growth factor receptor-beta (PDGFR-beta) subunit after vascular injury.

53 receptor 2 (VEGFR2) and PDGF receptor-beta (PDGFR-beta) were blunted in diabetic Prkcd(+/+) mice but

54 ed that LOX oxidizes the PDGF receptor-beta (PDGFR-beta), leading to amplified downstream signaling.

55 proteins, including the PDGF receptor-beta (PDGFR-beta), to affect PDGF-BB-induced chemotaxis.

56 latelet-derived growth factor receptor-beta (PDGFR-beta)-mediated signaling plays a key role in morph

57 or tyrosine kinases (RTKs), i.e. IGF1R-beta, PDGFR-beta, EGFR and c-MET, in colon, prostate, and brea

58 Blocking PDGFR-beta signaling did not prevent the differentiation

59 Both PDGFR-beta- and PDGFR-alpha-mediated pathways promote co

60 us, myointimal proliferation depends on both PDGFR-beta overexpression and its activation by PDGF-BB.

61 Pericyte coverage was determined by PDGFR-beta and alpha-SMA staining.

62 These results demonstrate that cardiomyocyte PDGFR-beta is a regulator of the compensatory cardiac re

63 echanistically, we showed that cardiomyocyte PDGFR-beta signaling plays a vital role in stress-induce

64 ifically, we demonstrated that cardiomyocyte PDGFR-beta was an essential upstream regulator of the st

65 ed PDGF-dependent cellular function, certain PDGFR-beta-induced signal cascades are not essential for

66 plasmic domain mutants of the chimeric M-CSF/PDGFR-beta, we confirmed that the kinase domain of PDGFR

67 skin is impaired, correlating with defective PDGFR-beta and transforming growth factor-beta (TGF-beta

68 Northern blot analysis failed to detect PDGFR-beta mRNA in mutant cells.

69 8 and M-CSF expression, but it downregulated PDGFR-beta.

70 EGF, TGF-alpha upregulated additional EGFR, PDGFR-beta, bFGF, and TGF-beta 1, suggesting that althou

71 me of the alpha SMA-positive cells expressed PDGFR beta, desmin, and neural/glial cell 2 (NG2), consi

72 2.5% of medial smooth muscle cells expressed PDGFR-beta.

73 s mitogenic for mesenchymal cells expressing PDGFR-beta, and PI3-K is an important regulator of PDGF-

74 othelial HS appears sufficient to facilitate PDGFR-beta activation in trans.

75 addition to the widely accepted function for PDGFR-beta in CDR formation, PDGFR-alpha is also clearly

76 ol/L) being more than 450-fold selective for PDGFR-beta versus other angiogenic receptors (e.g., vasc

77 These cells also express functional PDGFR beta, as demonstrated by autophosphorylation of th

78 telomestatin significantly reduced the human PDGFR-beta basal promoter activity relative to the contr

79 clease hypersensitivity element of the human PDGFR-beta gene promoter have been found to inhibit PDGF

80 d the first functional promoter of the human PDGFR-beta gene, which has been confirmed by luciferase

81 pecific G-quadruplex structures in the human PDGFR-beta promoter can modulate its transcription.

82 region (positions -165 to -139) of the human PDGFR-beta promoter is crucial for basal promoter activi

83 fferent G-quadruplex structures of the human PDGFR-beta promoter.

84 Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.

85 h the pericyte marker (immunohistochemistry: PDGFR-beta) and CK19.

86 rmined the NMR structure of the dGMP-fill-in PDGFR-beta vG4 in K(+) solution.

87 The G-quadruplexes (G4s) formed in PDGFR-beta gene promoter are transcriptional modulators

88 orphogenesis reminiscent of that observed in PDGFR-beta-/- mice with significantly reduced immunostai

89 indings indicate p.Arg561Cys substitution in PDGFR-beta as a cause of the dominant form of this disea

90 ndent signal transduction pathway, including PDGFR-beta, SHP2, AKT1, and ERK1/ERK2 (p44/42 MAPK), tur

91 ed by significant upregulation and increased PDGFR-beta signaling.

92 However, the importance of individual PDGFR-beta signal transduction pathways in vivo is not k

93 PDGF-BB with nanofibers induced PDGFR-beta and Akt phosphorylation in cardiomyocytes in

94 eta gene promoter have been found to inhibit PDGFR-beta transcriptional activity.

95 ic reporter mouse, we showed that inhibiting PDGFR-beta activation restricted the distribution of col

96 In this study, we localized PDGFR beta in the developing rat kidney and explored the

97 In all animals, medial PDGFR-beta expression doubled 2 weeks after endothelial

98 target this secondary structure and modulate PDGFR-beta gene expression.

99 -/- cells made to express "add-back" mutant PDGFR-beta capable of binding PI3-K.

100 the mutant mice that suggest that the mutant PDGFR-beta operates at suboptimal levels.

101 mutations in the genes SMARCA4, EPHA3, MYB, PDGFR-beta, and PIK3CA.

102 and extracellular ligand binding domains of PDGFR beta (exons 2-23) and c-kit (exons 1-21) in 6 pati

103 We have mapped Y740 as a site of PDGFR beta that is involved in the association with PSM.

104 RasGAP, that responds to activation of PDGFR-beta but not PDGFR-alpha, was not phosphorylated o

105 PDGF-AB ligand in the vigorous activation of PDGFR-beta homodimers to produce CDRs.

106 nd PDGF-BB-stimulated autophosphorylation of PDGFR-beta in cells (IC(50) = 1 nmol/L) being more than

107 GFR-beta) expression and the contribution of PDGFR-beta in neointimal formation.

108 beta, we confirmed that the kinase domain of PDGFR-beta is absolutely required for LRP tyrosine phosp

109 Aberrant expression of PDGFR-beta is associated with a number of diseases.

110 lmost completely abolished the expression of PDGFR-beta protein in the intima and media of injured ca

111 hese observations suggest that inhibition of PDGFR-beta might improve delivery of a concurrently admi

112 Inhibition of PDGFR-beta phosphorylation in tumors correlates with pla

113 ating TPH1 down-regulation via inhibition of PDGFR-beta signaling.

114 ukemic cells expressed much higher levels of PDGFR-beta transcripts than purified normal CD8(+) T cel

115 r metastatic potential, and higher levels of PDGFR-beta were expressed on cells with lower metastatic

116 These models include an ex vivo measure of PDGFR-beta phosphorylation in glioblastoma tumors, a spo

117 73,451 and to understand the pharmacology of PDGFR-beta inhibition and the effect on tumor growth.

118 nd preserving stemness-related properties of PDGFR-beta(+) MSCs, including the ability to repopulate

119 This study highlights the significance of PDGFR-beta signaling for the recruitment, proliferation,

120 PDGF-C(-/-) mice) or even an upregulation of PDGFR-beta and signaling (anti-PDGF-C group).

121 ies that are characterized by either abl- or PDGFR beta- activating mutations.

122 dy demonstrates that hematopoietic PDGF-B or PDGFR beta expression is not required for hematopoiesis

123 Mice deficient in PDGF B-chain or PDGFR beta exhibit an abnormal glomerular phenotype char

124 GFR-alpha (Ab-PDGFR-alpha; 10 mg/kg; n=5) or PDGFR-beta (Ab-PDGFR-beta; 10 mg/kg; n=6) by pulsed intr

125 ed by increased expression of PDGFR-alpha or PDGFR-beta in NSCLC cells.

126 thesis that inhibiting either PDGFR-alpha or PDGFR-beta with a specific mouse/human chimeric antibody

127 one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors, and most tumors

128 sults indicate that RGS5 exerts control over PDGFR-beta and GPCR-mediated signaling pathways active d

129 purified from control SMC contained oxidized PDGFR-beta.

130 ding of PDGF-BB by cells containing oxidized PDGFR-beta was diminished by approximately 2-fold when c

131 te markers in carcinoma cells, in particular PDGFR-beta and N-cadherin, which enabled EMT cells to be

132 Perivascular cells expressing phosphorylated PDGFR-beta were identified in the infarct after 7 days o

133 le formation, including podocalyxin (Podxl), PDGFR-beta, and a follistatin-domain-encoding gene Flst1

134 e shown that PDGF-D and its cognate receptor PDGFR-beta are expressed in prostate tumor tissues, sugg

135 essed by endothelial cells, and its receptor PDGFR-beta, expressed by pericytes, plays a central role

136 owth factor (PDGF)-B and PDGF beta-receptor (PDGFR beta) deficiency in mice is embryonic lethal and r

137 latelet-derived growth factor beta-receptor (PDGFR-beta) kinase- and PDGF-BB-stimulated autophosphory

138 of platelet-derived growth factor receptor (PDGFR-beta) was specifically downregulated in mutant fib

139 the platelet-derived growth factor receptor (PDGFR-beta).

140 ast growth factor receptors, VEGF receptors, PDGFR-beta, and c-KIT, as second-line therapy both in pa

141 otides to reduce PDGF-beta receptor subunit (PDGFR-beta) expression and the contribution of PDGFR-bet

142 Targeting PDGFR-beta may be an effective pharmacological strategy

143 studies of rat embryonic kidneys reveal that PDGFR beta localizes to undifferentiated metanephric mes

144 ed for LRP tyrosine phosphorylation but that PDGFR-beta-mediated activation of phosphatidylinositol 3

145 As described herein, we have found that PDGFR-beta expression and activation increase dramatical

146 Studies in animals have suggested that PDGFR-beta inhibition reduces tumor interstitial fluid p

147 The PDGFR-beta blockade resulted in impaired maturation of t

148 y the cellular compartment where LRP and the PDGFR-beta may interact, we employed immunofluorescence

149 The transcription initiation from the PDGFR-beta gene promoter was not significantly changed,

150 Furthermore, the PDGFR-beta mRNA level in Daoy cells was significantly de

151 The major G4 formed in the PDGFR-beta gene promoter was previously shown to have a

152 ium of 3'- and 5'-end vG4s is present in the PDGFR-beta promoter sequence, and dGMP favors the 5'-end

153 ermined the major G-quadruplex formed in the PDGFR-beta promoter.

154 Further, phosphorylated forms of the PDGFR-beta co-immunoprecipitated with LRP following PDGF

155 plays a specific role in the control of the PDGFR-beta expression.

156 quence related to a promoter sequence of the PDGFR-beta nuclease hypersensitivity element (NHE) compr

157 thelial cells in vitro via inhibition of the PDGFR-beta pathway.

158 The novel folding of the PDGFR-beta promoter G-quadruplex emphasizes the robustne

159 The novel folding of the PDGFR-beta promoter G-quadruplex may be attractive for s

160 or in which the ligand binding domain of the PDGFR-beta was replaced with that from the macrophage co

161 Phosphorylated members of the PDGFR-beta-dependent signal transduction pathway, includ

162 e rational design of ligands that target the PDGFR-beta vG4.

163 Herein, we report that the PDGFR-beta gene promoter sequence forms a vacancy G-quad

164 administering morphine or fentanyl with the PDGFR-beta inhibitor imatinib.

165 the potent migratory factor PDGF-BB through PDGFR-beta.

166 e oligonucleotide sequences complementary to PDGFR-beta mRNA almost completely abolished the expressi

167 Binding of PDGF to PDGFR-beta induces autophosphorylation at specific tyros

168 ly selective PDGFR inhibitor, inhibits tumor PDGFR-beta phosphorylation, selectively inhibits PDGF-BB

169 nt on PI3-K activation were determined using PDGFR-beta -/- cells made to express "add-back" mutant P

170 SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed i

171 ls initially enter the thymus at E13.5, with PDGFR-beta(+) mesenchymal cells following at E14.5.

172 a cell-autonomous manner, acting in cis with PDGFR-beta and TGF-beta receptors during induction/polar

173 und that wild-type LRP6 forms a complex with PDGFR-beta and enhances its lysosomal degradation, funct

174 ointimal formation correlated precisely with PDGFR-beta expression in an exponential fashion.