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 ring these predicted deleterious variants in KDR.

8 ane regions can each confer association with KDR.

9 providing evidence for direct involvement of KDR.

10 e receptor with strong homology to mammalian KDR.

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

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

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

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

15 -1,4-benzoxazines as inhibitors of intrinsic KDR activity (IC 50 < 0.1 microM) and human umbilical ve

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

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 fixed (>= 90%) in all villages but the 1575Y kdr-amplifying mutation was relatively rare (< 15%).

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

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

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 e transcription, positively of proangiogenic KDR and negatively, in part, of antiangiogenic SFRP4 Twi

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

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

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

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

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

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

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

61 These findings provide evidence for KDR being a clinically actionable PAH gene and further s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 KDR CNGs were also associated with significantly increas

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

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

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

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

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

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

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

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

96 phosphorylation and impairs VEGF-stimulated KDR degradation.

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

98 in shade avoidance; however, we propose that KDR does not interact with HFR1 to regulate shade avoida

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

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

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

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

103 3[G], OR=1.28; P=3.8 x 10(-11)), upstream of KDR encoding vascular endothelial growth factor receptor

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

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

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

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

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

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

110 KDR expression increased in myeloid cells as myeloid-der

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 The KDR gene, which participates in angiogenesis and lymphan

130 riants in the Kinase Insert Domain Receptor (KDR) gene were strongly associated with significantly re

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

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

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

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

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

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

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

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

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

140 Kdr heterozygote males were more likely to mate than hom

141 We demonstrate that KDR(hi)CD31(-) hematovascular mesodermal progenitors (HV

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

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

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

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

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

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

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

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

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

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

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

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

154 Here, we established roles of KDR in regulating shade avoidance in Arabidopsis (Arabid

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

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

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

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

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

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

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

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

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

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

165 We identified KDR interactors using a combination of yeast two-hybrid

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

167 We showed that KDR is a positive regulator of shade avoidance and inter

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

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

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

171 We demonstrated that KDR is translocated primarily to the nucleus when coexpr

172 2 (VEGFR-2 or kinase insert domain receptor; KDR) is a known endothelial target also expressed in NSC

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

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

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

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

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

178 Furthermore, KDR knockdown experiments using small interfering RNA re

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

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

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

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

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

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

185 VEGFR2-ephrinB2 compound mice (Nes-cre Kdr(lox/+) Efnb2(lox/+)) show reduced dendritic branchin

186 Mice lacking VEGFR2 in neurons (Nes-cre Kdr(lox/-)) show decreased dendritic arbors and spines a

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

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

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

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

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

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

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

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

195 enotyping revealed a high frequency of 1014F kdr mutation (82%) with significant difference in genoty

196 The 1014F kdr mutation was almost fixed (>= 90%) in all villages b

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

198 les gambiae sensu stricto homozygous for the kdr mutation.

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

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

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

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

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

204 The L1014F kdr-N1575Y haplotype and I1527T mutation were significan

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

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

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

208 6; P<0.001), suggesting a negative impact of kdr on An. coluzzii mating ability.

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

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

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

212 VEGF and its receptor VEGFR2 (also known as KDR or FLK1) are expressed in mouse hippocampal neurons

213 developing hippocampus VEGFR2 (also known as KDR or FLK1) is expressed specifically in the CA3 region

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

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

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

217 ances endothelial cell proliferation via the KDR pathway.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 KDR+ progenitors require active KDR signaling both to in

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

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

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

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

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

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

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

240 (Arabidopsis thaliana) and investigated how KDR regulates the shade avoidance network.

241 the distribution of the multiple origins of kdr resistance, finding unprecedented diversity in the D

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

243 brafish angioblasts by enhancing endothelial kdr sensitivity to VEGF.

244 ased or decreased colocalization of GFP with KDR/SFRP4 and CD31 in the regenerated diabetic wound bed

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

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

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

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

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

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

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

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

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

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

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

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

257 , regulating SMYD1 that activates HAND2, and KDR that with HAND2 orchestrates outflow tract formation

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

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

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

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

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

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

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

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

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

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

268 aled recurrently mutated genes that included KDR, TP53, and PIK3CA.

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

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

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

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

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

274 for familial segregation of a rare nonsense KDR variant with these phenotypes.

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

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

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

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

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

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

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

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

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

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

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

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

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

291 ith rare likely loss-of-function variants in KDR were independently identified in the US PAH Biobank

292 Another (b)HLH protein, KIDARI (KDR), which is non-DNA-binding, was identified in de-eti

293 pproach allowed us to independently validate KDR, which encodes for the Vascular Endothelial Growth F

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

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

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

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

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