ライフサイエンスコーパス: KDR

1 cells expressing the cardiac mesoderm marker KDR(+).

2 luorobutane-containing lipid-shelled MBs (MB(KDR)).

3 n of the VEGF receptor VEGFR2 (also known as KDR).

4 elial growth factor receptor-2 (VEGFR2/Flk-1/KDR).

5 ctor receptor-2 (VEGFR2/fetal liver kinase 1/KDR).

6 r methylation of VEGF genes (FLT4, FLT1, and KDR).

7 ane regions can each confer association with KDR.

8 providing evidence for direct involvement of KDR.

9 e receptor with strong homology to mammalian KDR.

10 High frequencies of L1014F kdr (75%) and Rdl (87%) mutations were observed showing

11 Silencing of ECSCR disrupts VEGF-induced KDR activation and AKT and ERK phosphorylation and impai

12 otein 2 (ID2) as a key upstream regulator of KDR activation during myeloid differentiation.

13 ctivation of KDR/PLCgamma1 signaling besides KDR activation in angiosarcomas, with implications for V

14 -1,4-benzoxazines as inhibitors of intrinsic KDR activity (IC 50 < 0.1 microM) and human umbilical ve

15 EPC counts (CD34/KDR) after 24 months were defined as primary endpoint.

16 sect strains, finding no correlation for the kdr allele at the genomic DNA level with levels of susce

17 ever, there was a strong correlation between kdr allele expression and the levels of insecticide resi

18 No 1014F or 1014S kdr alleles were detected in this population.

19 a systematic study of resistance-associated kdr allelic expression within and among resistant and su

20 Human MB(KDR) allow in vivo imaging and longitudinal monitoring o

21 scular endothelial growth factor-2 receptor, kdr (also known as kdra).

22 regulation of kinase insert domain receptor (KDR), also known as VEGFR2, in a myeloid cell sublineage

23 ater binding specificity of MB(KDR) to human KDR and cross-reactivity to murine VEGFR2 (P < or = .01)

24 Binding specificity of MB(KDR) to human KDR and cross-reactivity with murine vascular endothelia

25 angiopoietin-2 (Ang-2), CD31, and receptors KDR and CXCR2 in human umbilical vein endothelial cells.

26 also disrupted complexation between NRP1 and KDR and decreased VEGF-dependent phosphorylation of foca

27 sponding to the autophosphorylation sites of Kdr and developed a simple, robust, high-throughput assa

28 ontaining receptor (KDR) by associating with KDR and enhancing VEGF signaling.

29 essors (TGFBR1 and CHEK2) and two oncogenes (KDR and ERBB2).

30 r endothelial growth factor (VEGF) receptors KDR and Flt-1 at both the mRNA and protein levels.

31 of their expression blocked hypoxia-induced Kdr and Flt1 activation, respectively.

32 Hypoxia induced tyrosine phosphorylation of Kdr and Flt1 in mouse retina, and depletion of Kdr or Fl

33 indings suggest that although VEGFA, through Kdr and Flt1, appears to be the major modulator of Src-P

34 retinal neovascularization via activation of Kdr and Flt1, respectively.

35 wth factor A (VEGFA), we studied the role of Kdr and Flt1.

36 iated via complex formation between NRP1 and KDR and increased signaling to focal adhesions.

37 f multiple independent origins of kdr, super-kdr and kdr-his on an unprecedented geographic scale.

38 a small region of chromosome 4 encompassing KDR and KIT were identified by SNP array analysis.

39 s of ROR2(+) cells and diffuse expression of KDR and PDGFRalpha in first-trimester human fetal hearts

40 The EPCs (CD133(+)/KDR(+), CD34(+)/KDR(+)) and endothelial microparticles (EMPs: CD31(+)/CD

41 the growth factor receptors VEGFR-2 (Flk-1, KDR) and FGFR-1.

42 carrying both endothelial progenitor (CD34, KDR) and osteoblastic (osteocalcin [OCN]) cell surface m

43 ense mutations in the genes encoding VEGFR2 (KDR) and TEM8 (ANTXR1).

44 (PGF); VEGF receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4); and the gene encoding pigment e

45 oximately 2-fold) in the percentage of CD34+/KDR+ and CD34+/CD133+/KDR+ cells costaining for OCN.

46 er of circulating CD34+, CD34+/AC133+, CD34+/KDR+, and CD34+/AC133+/KDR+ progenitor cells was low in

47 enes involved in angiogenesis such as FLT-1, KDR, and angiopoietin 2 have potential E2F1 binding site

48 ls that coexpress PC antigens, such as CD34, KDR, and CXCR4.

49 ar endothelial growth factor (VEGF) receptor KDR, and genes involved in angiogenesis (LRP5, FZD4) on

50 VEGFA, KDR, and HMOX1 were associated with prolonged respirator

51 od mononuclear cells were analyzed for CD34, KDR, and OCN.

52 ed via its major signalling receptor, VEGFR2/KDR, and the protein kinase C (PKC) pathway.

53 vascular endothelial growth factor receptor KDR; and NTRK genes.

54 hrombin (vascular endothelial growth factor, KDR, Ang-2, matrix metalloproteinase 1, GRO-alpha, and C

55 Circulating EPCs (CD34(+)/KDR(+)), angiogenic T cells (CD3(+)/CD31(+)/CXCR4(+)), a

56 Compatible with these findings, a KDR antagonist blocked this response.

57 el and observed that both anti-VEGF and anti-KDR antibodies inhibit the transmigration of both CD4(+)

58 We found that WT1 and KDR are co-expressed in Sertoli cells of the testes and

59 ic mutations in Vssc (kdr, kdr-his and super-kdr) are known to cause resistance to pyrethroid insecti

60 ase results from a reduced potassium current Kdr as a result of accumulation of periaxonal potassium

61 To explore Kdr as an anticancer target and further characterize the

62 sponding to the autophosphorylation sites of Kdr as substrates for the enzyme has general practical i

63 Depletion of Kdr attenuated VEGFA-induced Src-PLD1-PKCgamma-cPLA2 act

64 domain-containing receptor tyrosine kinase (KDR) both enzymatically (<10 nM) and cellularly (<10 nM)

65 how that ECSCR biochemically associates with KDR but not FLT1 and that the predicted ECSCR cytoplasmi

66 show reduced VEGF-induced phosphorylation of KDR but not of FMS-like tyrosine kinase 1 (FLT1)/VEGF re

67 hESC-derived endoderm cells do not express KDR but, when cultured in media supporting hepatic diffe

68 F) receptor 2/kinase insert domain receptor (KDR) but not VEGF receptor 1/FLT1.

69 hibition of VEGF or VEGF receptor 2 (VEGFR2)/KDR, but not VEGFR1/Flt-1, was sufficient to abrogate VE

70 sions, and tissues were stained for CD31 and KDR by IHC.

71 or kinase insert domain-containing receptor (KDR) by associating with KDR and enhancing VEGF signalin

72 and endothelial cells)--Flk1 (also known as Kdr), c-Kit, and Nkx2-5, but not Brachyury--and subseque

73 After HiFI, the number of CD34+/KDR+-CACs, as measured by flow cytometry, increased 2.2-

74 ood pressure with increasing levels of CD34+/KDR+-CACs.

75 nsert domain protein receptor, also known as Kdr) cardiovascular progenitor that represents one of th

76 phosphate transfer activity of the purified Kdr-CD required Mg2+ or Mn2+ and preactivation by adenos

77 purified a cytoplasmic domain of human Kdr (Kdr-CD) and characterized its autophosphorylation activi

78 me activity; optimized the concentrations of Kdr-CD, peptide and ATP substrates, and metal ions in th

79 e hematopoietic mesoderm and WNT-independent KDR(+)CD235a(+) primitive hematopoietic mesoderm reveale

80 me gene expression analyses on WNT-dependent KDR(+)CD235a(-) definitive hematopoietic mesoderm and WN

81 exclusively within definitive hematopoietic KDR(+)CD235a(-) mesoderm in a WNT- and fibroblast growth

82 The EPCs (CD133(+)/KDR(+), CD34(+)/KDR(+)) and endothelial microparticles (

83 identified as CD49f(H) CD41(H) (and c-Kit(D)KDR(+)CD42(+)CD9(++)CD31(+)) cells, expressing several h

84 ctrical resistance (TER), of PAE/Npn and PAE/KDR cell lines was not altered by VEGF165.

85 B19V DNA concentrations were found in CD34(+)KDR(+) cells from 17 patients with chronic B19V-associat

86 s patients in the percentage of CD34+/CD133-/KDR+ cells costaining for OCN (5- and 2-fold, p < 0.001

87 he percentage of CD34+/KDR+ and CD34+/CD133+/KDR+ cells costaining for OCN.

88 simulating three scenarios of AngII-mediated KDR channel phosphorylation: (1), an increased steady st

89 ngiogenesis, and HIF-1alpha levels, and that KDR CNGs may be a useful biomarker for identifying patie

90 Our findings suggest that tumor cell KDR CNGs may promote a more malignant phenotype includin

91 KDR CNGs were also associated with significantly increas

92 we assessed NSCLC cell lines and found that KDR CNGs were significantly associated with in vitro res

93 tion, and HIF-1alpha levels in cells bearing KDR CNGs, providing evidence for direct involvement of K

94 We also found that KDR colocalizes with CD3 on mitogen-activated T cells in

95 re than three times higher (P = .01) with MB(KDR) compared with control MBs and decreased significant

96 F165 rapidly and transiently increases ECSCR-KDR complex formation, a process blocked by the KDR tyro

97 The depletion of myeloid-derived KDR compromised its proangiogenic function, which inhibi

98 KDR copy number gains (CNG), measured by quantitative PC

99 KDR deficiency in murine BM-derived cells (BMDCs) suppre

100 phosphorylation and impairs VEGF-stimulated KDR degradation.

101 rafts, interferes with VEGFR2 (also known as KDR) dimerization and signalling and inhibits vascular e

102 nd tube formation, albeit more robustly with Kdr downregulation.

103 Flt4, a receptor for Vegfc, cooperates with Kdr during artery morphogenesis, but not differentiation

104 le labeling experiments show VEGF-stimulated KDR(+)/ECSCR(+) intracellular co-localization.

105 esion contained a single somatic mutation in KDR (encodes VEGFR2), possibly in response to ramuciruma

106 3[G], OR=1.28; P=3.8 x 10(-11)), upstream of KDR encoding vascular endothelial growth factor receptor

107 CD34(+) population from CD34(+)CD43(-)CD31(+)KDR(+) endothelial and CD34(+)CD43(-)CD31(-)KDR(-) mesen

108 CD133+CD34+KDR+ endothelial cell progenitor cells emigrate from the

109 d CD235a; 2) anti-CD144 (EC marker) and anti-KDR (EPC marker) conjugated-Q-dots exhibited the best se

110 der this condition, suggesting a role of the KDR-ERK1/2 pathway on endothelial cell proliferation.

111 ial cell proliferation via activation of the KDR-ERK1/2 pathway.

112 the bone marrow and differentiate into CD34+KDR+ expressing cells, which are present in high numbers

113 del of lymphocyte trafficking, we found that KDR-expressing lymphocytes migrate into human skin in vi

114 ction of KDR on each T cell subset, and that KDR-expressing lymphocytes preferentially transmigrate a

115 ur findings suggest that dynamin-2 regulates KDR expression and function and hence plays an important

116 cells were largely devoid of VE-cadherin and KDR expression and had a distinct FLT3(high)GATA3(low)RU

117 KDR expression increased in myeloid cells as myeloid-der

118 ng the 40 patients included in the analysis, KDR expression on IHC matched well with imaging signal o

119 d KDR-targeted USMI signal matches well with KDR expression on IHC.

120 he DH GRN through gata2 expression, then for kdr expression to enable the DH to respond to vascular e

121 using MBKDR is safe and allows assessment of KDR expression using immunohistochemistry (IHC) as the g

122 l oxygen environment and WT1, which enhances KDR expression, contribute to sex-specific Sox9 expressi

123 or complex with Flt-1 (VEGFR1), but not with KDR/Flk-1 (VEGFR2) or with Flt-4 (VEGFR3).

124 Expression of VEGF-receptor2/KDR/Flk-1 was confirmed with Western blot and immunostai

125 ndothelial growth factor receptor-2 (VEGFR-2/KDR/flk-1) functions as the primary mediator of vascular

126 l growth factor (VEGF), and VEGF receptor-2 (KDR/Flk-1), Peroxisome proliferator-activated receptor g

127 endothelial cell-adhesion molecule-1, CD34, KDR/Flk-1, vascular endothelial cadherin, von Willebrand

128 EGF receptor-1 (VEGFR-1; Flt-1) and VEGFR-2 (KDR; Flk-1) (VEGFR(1-2)) in endothelial cells with a syn

129 , and a duplicate RTK locus with homology to KDR/FLK1 (named Kdrb).

130 helial growth factor (VEGF) receptor (VEGFR2/KDR/Flk1) on the endothelial cell surface.

131 augments vascular SMC migration via VEGFR2 (KDR/Flk1) pathways.

132 mplex to cardiomyogenic loci in multipotent (KDR/Flk1+) progenitors, activating lineage-specific tran

133 PDGFRalpha(-) cells are characterized by Kdr/Flk1, Cdh5, CD31 and lack of clonogenicity.

134 ected is a target-site knock-down resistance kdr-form, on a background of generally elevated metaboli

135 d the association between alterations in the KDR gene and clinical outcome in patients with resected

136 Polymorphisms in the VEGFR2/KDR gene significantly influence visual outcome in patie

137 The KDR gene, which participates in angiogenesis and lymphan

138 mediated active transcription of the VEGFR2 (KDR) gene.

139 n upstream sequences of mouse flk1 and human kdr genes, suggesting that the regulatory machinery for

140 We assert that the link between kdr genotype and DDT- and pyrethroid-susceptibility phen

141 However, we emphasize that kdr genotype might explain only a portion of heritable v

142 ave concluded that the knockdown resistance (kdr) genotype-phenotype correlation that is observed in

143 acing in mice provides in vivo evidence of a KDR+ hepatic progenitor for fetal hepatoblasts, adult he

144 supporting hepatic differentiation, generate KDR+ hepatic progenitors and KDR- hepatic cells.

145 ation, generate KDR+ hepatic progenitors and KDR- hepatic cells.

146 port the functional maturation of cocultured KDR- hepatic cells.

147 Kdr heterozygote males were more likely to mate than hom

148 These results provide evidence that a VEGF/KDR/HIF-1 alpha autocrine loop differentially mediates s

149 Specific mutations in Vssc (kdr, kdr-his and super-kdr) are known to cause resistance to

150 e the number of evolutionary origins of kdr, kdr-his and super-kdr, we sequenced a region of Vssc fro

151 le independent origins of kdr, super-kdr and kdr-his on an unprecedented geographic scale.

152 A kinase insert domain-containing receptor (KDR) homology model suggests that these compounds bind t

153 ost on mosquitoes by reducing the ability of kdr homozygous A. gambiae sensu stricto to survive expos

154 Results showed that kdr homozygous mosquitoes that fed on infectious blood w

155 ulocyte-macrophage CSF (GM-CSF) enhanced the KDR/ID2 signaling axis in BMDCs.

156 Our results suggest that modulation of KDR/ID2 signaling may restrict tumor-associated myeloid

157 st time define a novel function for VEGF and KDR in CD45RO+ memory T cell responses that are likely o

158 Deletion of Kdr in DCs resulted in reduced production of type I inte

159 The involvement of KDR in endometriosis risk highlights the importance of t

160 d to achieve prolonged inhibition of Kit and KDR in humans and which would therefore be expected to y

161 identified as potent inhibitors of VEGFR-2 (KDR) in both enzymatic and HUVEC cellular proliferation

162 Expression of VEGF receptor-2 (KDR) in OECs after expansion was determined by Western b

163 In addition, a VEGF mutant, which binds only KDR, induced extracellular signal-regulated kinase (ERK)

164 ed the stimulatory effect of SU1498-mediated KDR inhibition on Sox9 expression.

165 T cell line and by SU5416, a pharmacological KDR inhibitor, in CD4+CD45RO+ T cells.

166 n the basis of X-ray cocrystal structures of KDR inhibitors 34 (triazine) and 35 (nicotinamide).

167 the kinase, which was inhibited by specific KDR inhibitors.

168 riphosphate (ATP) and was inhibited by known Kdr inhibitors.

169 and ATP as well as IC50 values of two known Kdr inhibitors.

170 s ECSCR protein, suggesting a role for ECSCR-KDR interaction in these tissues.

171 Altogether, our findings reveal that KDR is a conserved marker for endoderm-derived hepatic p

172 latent polyadenylation site in intron 13 of KDR is activated by blocking the upstream 5' splicing si

173 sting that the regulatory machinery for flk1/kdr is conserved from fish to mammals.

174 ar endothelial growth factor (VEGF) receptor KDR is expressed on subsets of mitogen-activated CD4(+)

175 2 (VEGFR-2 or kinase insert domain receptor; KDR) is a known endothelial target also expressed in NSC

176 ing of EXEL-2880 to Met and VEGF receptor 2 (KDR) is characterized by a very slow off-rate, consisten

177 ls, where an additional layer of resistance (kdr) is possible.

178 e, we purified a cytoplasmic domain of human Kdr (Kdr-CD) and characterized its autophosphorylation a

179 Specific mutations in Vssc (kdr, kdr-his and super-kdr) are known to cause resistanc

180 ermine the number of evolutionary origins of kdr, kdr-his and super-kdr, we sequenced a region of Vss

181 Optimization of those compounds as KDR kinase inhibitors identified 8, which displayed an o

182 Furthermore, KDR knockdown experiments using small interfering RNA re

183 d lower concentration of circulating CD34(+)/KDR(+) levels.

184 KDR tyrosine kinase inhibitor SU1498 or the KDR ligand VEGFA revealed that KDR signaling represses t

185 ish Vegf receptor-2 ortholog (referred to as kdr-like, kdrl) revealed surprisingly varied effects on

186 stem-cell-derived embryoid bodies generate a KDR(low)/C-KIT(CD117)(neg) population that displays card

187 When plated in monolayer cultures, these KDR(low)/C-KIT(neg) cells differentiate to generate popu

188 Populations derived from the KDR(low)/C-KIT(neg) fraction give rise to colonies that

189 tide polymorphisms in the CFH, ARMS2, VEGFA, KDR, LPR5, and FZD4 genes was performed.

190 lly, compound 16 was identified as a potent (KDR: < 1 nM and HUVEC: 4 nM) and selective inhibitor tha

191 ly distinct protein products, membrane-bound KDR (mbKDR) and its isoform, soluble KDR (sKDR).

192 about the role of the knockdown resistance (kdr) mechanism.

193 To evaluate whether VEGF and KDR mediate lymphocyte migration across endothelial cell

194 molecular basis underlying the genotype and kdr-mediated resistance phenotype relationship.

195 Kdr-mediated signaling plays an important role in the pr

196 )KDR(+) endothelial and CD34(+)CD43(-)CD31(-)KDR(-) mesenchymal cells.

197 nctions as a transcription factor, increased KDR mRNA levels, whereas the WT1(+KTS) isoform, which ac

198 Transient transfection of KDR mutants into COS-7 cells showed ligand-independent a

199 leucine to phenylalanine, termed the L-to-F kdr mutation, in the sodium channel of the insect nervou

200 les gambiae sensu stricto homozygous for the kdr mutation.

201 ed PyR1 models explained recently discovered kdr mutations and predicted new deltamethrin-channel con

202 major role played by P450 in the absence of kdr mutations suggests that addition of the synergist PB

203 No KDR mutations were detected in exons 7, 11, and 21 by PC

204 e genes identified 10% of patients harboring KDR mutations.

205 China found that both knockdown resistance (kdr) mutations and monooxygenase activity were significa

206 In contrast, neither CD34(+)/KDR(+) nor CD34(+) variation was associated with signifi

207 Our signaling experiments show that KDR not Flt-1 mediated PKD tyrosine phosphorylation and

208 gnificantly higher numbers of EPC-OCN (CD34+/KDR+/OCN+) than controls.

209 sAS/sCAD had significantly less EPCs (CD34+/KDR+/OCN-) than controls.

210 6; P<0.001), suggesting a negative impact of kdr on An. coluzzii mating ability.

211 pha-activated ECs result in the induction of KDR on each T cell subset, and that KDR-expressing lymph

212 tions demonstrate that induced expression of KDR on subsets of T cells, and locally expressed VEGF, f

213 or kinase insert domain-containing receptor (Kdr), on the surface of endothelial cells.

214 microbubble [MBKDR]) that is targeted at the KDR, one of the key regulators of neoangiogenesis in can

215 r and Flt1 in mouse retina, and depletion of Kdr or Flt1 blocked hypoxia-induced Src-PLD1-PKCgamma-cP

216 ine with these findings, depletion of either Kdr or Flt1 suppressed VEGFA-induced DNA synthesis, migr

217 th greater than 200-fold selectivity against KDR, p38, Lck, and Src.

218 ances endothelial cell proliferation via the KDR pathway.

219 End2 cells greatly promotes the induction of KDR(+) PDGFRa(+) CPCs from human ES cells.

220 a population of hESC-derived ROR2(+)/CD13(+)/KDR(+)/PDGFRalpha(+) cells that give rise to cardiomyocy

221 ROR2(+)/CD13(+)/KDR(+)/PDGFRalpha(+) cells were delivered into these fun

222 Thus, hPS cell-derived KDR(-)PDGFRalpha(+ )paraxial mesoderm-like cells have po

223 Isolated (GFP(+))KDR(-)PDGFRalpha(+) mesoderm cells were sensitive to seq

224 Here we report the successful generation of KDR(-)PDGFRalpha(+) progeny expressing paraxial mesoderm

225 and stellate cells by way of reduced VEGFR2 (KDR), phospholipase Cgamma (PLCgamma), and extracellular

226 g no effect on Flt1 phosphorylation, induced Kdr phosphorylation in human retinal microvascular endot

227 epresent an alternative way of activation of KDR/PLCgamma1 signaling besides KDR activation in angios

228 A KDR-positive genotype was associated with strong KDR pro

229 ucturally, vascular niches composed of c-kit-KDR-positive VPCs were identified within the walls of co

230 , CD34+/AC133+, CD34+/KDR+, and CD34+/AC133+/KDR+ progenitor cells was low in Eisenmenger patients co

231 formation of cardiomyocytes from multipotent Kdr(+) progenitors while promoting the differentiation o

232 the formation of multipotent cardiovascular Kdr(+) progenitors.

233 KDR+ progenitors require active KDR signaling both to in

234 Furthermore, WT1 bound to the Kdr promoter in the chromatin of embryonic testes and ov

235 t WT1(-KTS), but not WT1(+KTS), binds to the KDR promoter.

236 ors and associated with significantly higher KDR protein and higher microvessel density than tumors w

237 positive genotype was associated with strong KDR protein expression and was restricted to the breast

238 ding (K44A) caused a selective inhibition in KDR protein level and endosomal vesicle formation and in

239 de resistant population exhibited high 1014F kdr(R) allele frequencies (>60%) and RDL(R) (>80%) in co

240 ge was detected in male homozygotes for both kdr/RDL-resistant alleles.

241 locking VEGF-mediated signaling by the Flk-1/KDR receptor kinase inhibitor SU5416 significantly inhib

242 iation-related factors, including Brachyury, KDR, SCL, GATA2, and PU.1.

243 brafish angioblasts by enhancing endothelial kdr sensitivity to VEGF.

244 KDR+ progenitors require active KDR signaling both to instruct their own differentiation

245 SU1498 or the KDR ligand VEGFA revealed that KDR signaling represses the testis-promoting gene Sox9 i

246 Neuropilin-1 (NRP-1)-mediated activation of KDR signaling through VEGF165 as a critical mechanism fo

247 e-bound KDR (mbKDR) and its isoform, soluble KDR (sKDR).

248 c receptor tyrosine kinases, including TIE1, KDR, SNRK, TEK, and FLT1.

249 ated signaling responses were inhibited by a KDR-specific small interfering RNA in a VEGF receptor-ex

250 ypothesis of multiple independent origins of kdr, super-kdr and kdr-his on an unprecedented geographi

251 ncy of ID2 in BMDCs led to downregulation of KDR, suppression of proangiogenic myeloid cells, and pre

252 in angiosarcomas, with implications for VEGF/KDR targeted therapies.

253 h MBKDR is clinically feasible and safe, and KDR-targeted USMI signal matches well with KDR expressio

254 Strong KDR-targeted USMI signal was present in 77% of malignant

255 ntrast agent (kinase insert domain receptor [KDR] -targeted contrast microbubble [MBKDR]) that is tar

256 eptor targeting the VEGF receptor-2 (VEGFR2; KDR) that is overexpressed on tumor vasculature and T-ce

257 we report that WT1 stimulates expression of Kdr, the gene encoding VEGF receptor 2, in murine embryo

258 pression and that it occurs independently of KDR, the main VEGF receptor in blood vessels.

259 endothelial growth factor receptor-2 (VEGFR2/KDR) to a dominant-negative sKDR results in a strong ant

260 four times greater binding specificity of MB(KDR) to human KDR and cross-reactivity to murine VEGFR2

261 Binding specificity of MB(KDR) to human KDR and cross-reactivity with murine vascu

262 sodium channels confer knockdown resistance (kdr) to pyrethroids, the atomic mechanisms of pyrethroid

263 ce and contribution of knockdown resistance (kdr) to pyrethroids/DDT resistance observed in Anopheles

264 In vivo binding specificity of MB(KDR) to VEGFR2 was tested in human LS174T colon cancer x

265 (CD34, CD133, kinase insert domain receptor [KDR]) to identify EPCs, we examined whether patients wit

266 Failure of VEGF receptor-2/KDR transactivation by extracellular nucleotides on CD39

267 -morpholino-mediated WT1 knockdown decreased Kdr transcripts in cultured embryonic gonads at multiple

268 complex formation, a process blocked by the KDR tyrosine kinase inhibitor compound SU5416 or inhibit

269 Treatment with the KDR tyrosine kinase inhibitor SU1498 or the KDR ligand V

270 -1 mediated PKD tyrosine phosphorylation and KDR tyrosine residues 951 and 1059 were required for VEG

271 s of potent inhibitors of the VEGF-R2 (flk-1/KDR) tyrosine kinase.

272 EGFR-2 or the kinase insert domain receptor (KDR) upon stimulation by its ligand VEGF.

273 s were sorted for c-kit (mCSCs) or c-kit and KDR (vCSCs) and characterized.

274 lineage-specific markers (Lin(-)), expressed KDR, VE-cadherin, and CD105 endothelial proteins, and ex

275 ated VEGF and kinase-insert domain receptor (KDR) (VEGF receptor 2) mRNA expression in BAEC.

276 e kinases VEGFR-1 (Flt-1) and VEGFR-2 (Flk-1/KDR), VEGF-B and PlGF bind to VEGFR-1 and not VEGFR-2.

277 with kinase insert domain protein receptor (KDR)/VEGF receptor 2 in these regions.

278 s receptors, Flt-1/FLT-1 (VEGFR-1) and Flk-1/KDR (VEGFR-2), are key regulators of tumor angiogenesis

279 e phosphorylation of the VEGF receptor Flk-1/KDR (VEGFR-2).

280 me "canalogenesis." Functional inhibition of KDR (VEGFR2), a critical receptor in initiating angiogen

281 Here, we show that KDR (VEGFR2/FLK-1), previously assumed to be mostly rest

282 nephron, whereas expression of its receptor (Kdr/Vegfr2) is largely restricted to adjacent peritubula

283 in chronic hypoxia (e.g. VEGFA, FLT1/VEGFR1, KDR/VEGFR2, BNIP3L, and SLC2A1/GLUT1), the function of w

284 biology and angiogenesis, such as TEK/Tie-2, KDR/VEGFR2, Tie-1, endothelial nitric oxide synthase and

285 usion between kinase insert domain receptor (KDR) (VEGFRII) and the PDGFRA gene, and six cases of PDG

286 racterized by the expression of VE-cadherin, KDR, von Willebrand factor, endothelial nitric oxide syn

287 the miR-200b gene targets ZEB1/2, GATA2, and KDR was confirmed by qRT-PCR as being lower in obese pat

288 of OEC clusters, expanded OECs and levels of KDR was demonstrated.

289 erial-enhanced US imaging signal by using MB(KDR) was longitudinally measured during 6 days in tumors

290 scular endothelial growth-factor receptor 2 (KDR) was used, together with the stem cell antigen c-kit

291 olutionary origins of kdr, kdr-his and super-kdr, we sequenced a region of Vssc from house flies coll

292 nases Kit and kinase insert domain receptor (KDR), which is currently being evaluated in clinical stu

293 , including Tlr7, Tlr9 and Nfkb1, as well as Kdr, which encodes the growth factor receptor VEGFR2.

294 atedly mutated genes identified by tNGS were KDR with different nonsynonymous mutations, MLL2 with di

295 , nor PlGF, induce the interaction of VEGFR2/KDR with IGF-1R, resulting in IGF-1R transactivation to

296 A heterodimeric peptide that binds to human KDR with low nanomolar affinity (K(D) = 0.5 nmol/L) was

297 OSI-930 selectively inhibits Kit and KDR with similar potency in intact cells and also inhibi

298 nd to yield nanomolar inhibitors of VEGFR-2 (KDR) with an improved selectivity profile against a pane

299 ptor 2/kinase insert domain receptor (VEGFR2/KDR) with IGF-1R, which mediates the expression of TR3-T

300 shin revealed a somatic p.T771R mutation in KDR, without evidence of other somatic mutations or loss