HUGO ID Detailed Result 6307


HUGO ID 6307
Symbol KDR
Name kinase insert domain receptor (a type III receptor tyrosine kinase)
#Occurrence 73
#Paper 1

 


PMID Match String Actual String Score Flanking text Edited by Edit
16104843VEGFRVEGFRs3.0is the VEGF (vascular vascular endothelial growth factor family and VEGFRs (VEGF VEGF receptors 
16104843VEGFR2VEGFR-24.3VEGFR-1 also known as Flt-1 (Fms-like Fms-like tyrosine kinase-1 and VEGFR-2 also known as Flk-1 (fetal fetal liver kinase-1 and in 
16104843FLK1Flk-13.0Flt-1 (Fms-like Fms-like tyrosine kinase-1 and VEGFR-2 also known as Flk-1 (fetal fetal liver kinase-1 and in humans as KDR (kinase 
16104843KDRKDR3.0as Flk-1 (fetal fetal liver kinase-1 and in humans as KDR (kinase kinase insert domain-containing receptor 3-5 
16104843VEGFRVEGFR3.3functions and the precise molecular mechanisms of the VEGF/VEGFR VEGF VEGFR system 
16104843VEGFRVEGFR3.3recent advances in the basic biology of the VEGF/VEGFR VEGF VEGFR system which give insight into many physiological and pathological conditions 
16104843VEGFR2VEGFR-24.3b is an endogenous inhibitory form of VEGF which binds VEGFR-2 with the same affinity as VEGF 165 but does not 
16104843VEGFR2VEGFR-24.3PlGF binds VEGFR-1 but not VEGFR-2 35 36 
16104843VEGFRVEGFR3.3bind and activate VEGFR-3 (Flt-4; Flt-4 a member of the VEGFR family that does not bind VEGF-A as well as VEGFR-2 
16104843VEGFR2VEGFR-24.3VEGFR family that does not bind VEGF-A as well as VEGFR-2 and are mitogenic for cultured endothelial cells 
16104843VEGFR2VEGFR-24.3the fully processed form with a high affinity for both VEGFR-2 and VEGFR-3 49 
16104843VEGFR2VEGFR-24.3All VEGF-E variants studied bind and activate VEGFR-2 but not VEGFR-1 or VEGFR-3 
16104843VEGFR2VEGFR-24.3Vammin does not bind VEGFR-1 but binds VEGFR-2 with high affinity as well as VEGF 165 64 
16104843VEGFR2VEGFR-24.3However Tf svVEGF binds VEGFR-1 with high affinity and VEGFR-2 with low affinity compared with VEGF 165 leading to a 
16104843VEGFRVEGFRs3.0VEGFRs 
16104843VEGFR2VEGFR-24.3VEGFR-1 binds VEGF-A with at least 10-fold higher affinity than VEGFR-2 ( K d =10-30 pM 16 however ligand binding results 
16104843VEGFR2VEGFR-24.3In many cases the effects of VEGFR-2 on endothelial cells such as those on cell survival and 
16104843VEGFRVEGFR-1-blocking3.0VEGFR-1-blocking antibodies prevent the migration but not proliferation of HUVECs (human 
16104843VEGFR2VEGFR-24.3of actin via p38 MAPK (mitogen-activated mitogen-activated protein kinase whereas VEGFR-2 contributes to the re-organization of the cytoskeleton by phosphorylating FAK 
16104843VEGFR2VEGFR-24.3VEGF-A from signalling receptors and by forming non-signalling heterodimers with VEGFR-2 69 
16104843VEGFR2VEGFR-24.3VEGFR-2 
16104843VEGFR2VEGFR-24.3VEGFR-2 is a 200-230 kDa high-affinity receptor for VEGF-A ( K 
16104843VEGFR2VEGFR-24.3VEGFR-2 is expressed in vascular and lymphatic endothelial cells and other 
16104843VEGFR2VEGFR-24.3Tyrosine phosphorylation sites in human VEGFR-2 bound to VEGF-A are Tyr and Tyr in the kinase-insert 
16104843VEGFRVEGFR-associated3.5Tyr creates a binding site for the VEGFR-associated protein 77 and Tyr creates a binding site for Sck 
16104843VEGFR2VEGFR-24.3VEGFR-2 is the major mediator of the mitogenic angiogenic and permeability-enhancing 
16104843VEGFR2VEGFR-24.3Furthermore recent studies have indicated that the activation of VEGFR-2 also promotes lymphangiogenesis 80 81 
16104843VEGFR2VEGFR-24.3Survival signalling for endothelial cells from VEGFR-2 is reported to involve the PI3K (phosphoinositide phosphoinositide 3-kinase)/Akt 3-kinase 
16104843VEGFR2VEGFR-24.3may be involved since the signal to activate PI3K by VEGFR-2 is usually not very strong 
16104843VEGFR2VEGFR-24.3Byzova et al 84 have reported that the activation of VEGFR-2 by VEGF-A results in the PI3K/Akt-dependent PI3K Akt-dependent activation of 
16104843VEGFR2VEGFR-24.3synergic interaction with integrins is required for productive signalling from VEGFR-2 
16104843VEGFR2VEGFR-24.3Very recently a naturally occurring soluble truncated form of VEGFR-2 has been detected in mouse and human plasma 85 
16104843VEGFR2VEGFR-24.3Similar to sVEGFR-1 sVEGFR-2 (soluble soluble VEGFR-2 may have regulatory consequences with respect to VEGF-mediated angiogenesis 
16104843VEGFR2VEGFR-24.3Unlike VEGFR-1 and VEGFR-2 VEGFR-3 is proteolytically cleaved within the fifth extracellular Ig loop 
16104843VEGFR2VEGFR-24.3VEGF 165 -induced proliferation and migration of cells that express VEGFR-2 are enhanced in the presence of NRP-1 
16104843VEGFR2VEGFR-24.3Thus NRP-1 also seems to function as an enhancer of VEGFR-2 activity in the presence of VEGF 165 
16104843VEGFR2VEGFR-24.3is the result of the formation of a complex between VEGFR-2 and NRP-1 93 94 
16104843VEGFRVEGFR3.3VEGF/VEGFR VEGF VEGFR SYSTEM IN PHYSIOLOGICAL AND PATHOLOGICAL CONDITIONS 
16104843VEGFR2VEGFR-24.3Homozygous loss of the VEGFR-1 or VEGFR-2 gene results in embryonic lethality between days 8.5 and 9.5 
16104843VEGFRVEGFRs3.0embryonic lethality between days 8.5 and 9.5 indicating that these VEGFRs play important roles in vasculogenesis and angiogenesis 101 102 
16104843VEGFR2VEGFR-24.3VEGFR-2 mice die due to a lack of endothelial cell growth 
16104843VEGFR2VEGFR-24.3the tyrosine kinase domain of VEGFR-1 103 has indicated that VEGFR-2 is the major positive signal transducer whereas VEGFR-1 has a 
16104843VEGFR2VEGFR-24.3Tyr and Tyr are two major VEGF-A-dependent autophosphorylation sites in VEGFR-2 
16104843VEGFR2VEGFR-24.3An unusual feature of mitogenic signalling from VEGFR-2 is the requirement for PKC but not Ras 104 
16104843VEGFR2VEGFR-24.3knockin mice substituting Tyr (corresponding corresponding to Tyr in human VEGFR-2 and Tyr (Tyr Tyr in human of the VEGFR-2 gene 
16104843VEGFR2VEGFR-24.3human VEGFR-2 and Tyr (Tyr Tyr in human of the VEGFR-2 gene with phenylalanine has revealed that the signalling via Tyr 
16104843VEGFR2VEGFR-24.3with phenylalanine has revealed that the signalling via Tyr of VEGFR-2 is essential for endothelial and haematopoietic development during embryogenesis 
16104843VEGFR2VEGFR-24.3the PI3K/p70 PI3K p70 S6K (S6 S6 kinase pathway by VEGFR-2 is also involved in VEGF-A-induced endothelial cell proliferation 107 ( 
16104843VEGFR2VEGFR-24.3VEGF-A increases vascular permeability in mesenteric microvessels by activation of VEGFR-2 on endothelial cells and subsequent activation of PLC 
16104843VEGFR2VEGFR-24.3Other studies have also demonstrated the crucial role of VEGFR-2 signalling in the enhancement of vascular permeability however our recent 
16104843VEGFR2VEGFR-24.3the proliferation of endothelial cells under some active signalling from VEGFR-2 
16104843VEGFR2VEGFR-24.3blockade of Src prevents the disassociation of a complex comprising VEGFR-2 VE-cadherin and b -catenin with the same kinetics with which 
16104843VEGFR2VEGFR-24.3enhancement of vascular permeability through the disruption of the VEGFR-2/cadherin/catenin VEGFR-2 cadherin catenin complex 
16104843VEGFR2VEGFR-24.3hypothesis capturing of VEGF or blocking of its signalling receptor VEGFR-2 by a VEGFR tyrosine kinase inhibitor antisense oligonucleotides vaccination or 
16104843VEGFRVEGFR3.3VEGF or blocking of its signalling receptor VEGFR-2 by a VEGFR tyrosine kinase inhibitor antisense oligonucleotides vaccination or neutralizing antibodies reduced 
16104843VEGFR2VEGFR-24.3that PlGF regulates inter- and intra-molecular cross-talk between VEGFR-1 and VEGFR-2 amplifying VEGF-driven angiogenesis through VEGFR-2 
16104843VEGFR2VEGFR-24.3intra-molecular cross-talk between VEGFR-1 and VEGFR-2 amplifying VEGF-driven angiogenesis through VEGFR-2 
16104843VEGFRVEGFRs3.0VEGF-A and VEGFRs are constitutively expressed in the islet vasculature before and after 
16104843VEGFR2VEGFR-24.3Pharmacological blockade of VEGFR-2 stabilizes the endothelial barrier function and suppresses tumour cell extravasation 
16104843VEGFR2VEGFR-24.3tumour cell extravasation in vivo 136 suggesting the importance of VEGFR-2 signalling in this kind of tumour invasion and metastasis 
16104843VEGFR2VEGFR-24.3165 promotes survival of motor neurons during hypoxia through binding VEGFR-2 and NRP-1 161 
16104843VEGFRVEGFR3.3evidence has revealed that the role of the VEGF/VEGFR VEGF VEGFR system extends far beyond previous expectations 
16104843VEGFRVEGFRs3.0Secondly several different VEGFRs have been shown to be essential but the interaction between 
16104843VEGFR2VEGFR-24.3signal transducer in some cases individually and sometimes synergistically with VEGFR-2 via the intra- and inter-molecular cross-talk between these two receptors 
16104843VEGFR2VEGFR-24.3An association between VEGFR-2 and VEGFR-3 has also been reported 166 
16104843VEGFRVEGFR3.3Thirdly it has been shown that the VEGF/VEGFR VEGF VEGFR system has multiple functions such as the induction of tumour 
16104843VEGFRVEGFR3.3molecules have been found to associate with the VEGF/VEGFR VEGF VEGFR system 
16104843VEGFRVEGFR3.3required to achieve a comprehensive understanding of the VEGF/VEGFR VEGF VEGFR system however the recent progress in the molecular and biological 
16104843VEGFRVEGFR3.3type 2 UTR untranslated region VEGF vascular endothelial growth factor VEGFR VEGF receptor sVEGFR-1 soluble VEGFR-1 svVEGF snake venom VEGF Tf 
16104843VEGFRVEGFR3.3VEGF-A binds to and activates two tyrosine kinase receptors VEGFR (VEGF VEGF receptor -1 and VEGFR-2 
16104843VEGFR2VEGFR-24.3two tyrosine kinase receptors VEGFR (VEGF VEGF receptor -1 and VEGFR-2 
16104843VEGFR2VEGFR-24.3VEGFR-2 mediates most of the endothelial growth and survival signals but 
16104843VEGFRVEGFR3.3in the molecular and biological understanding of the VEGF/VEGFR VEGF VEGFR system provides us with novel and promising therapeutic strategies and