HUGO ID Detailed Result 12680

PMID	Match String	Actual String	Score	Flanking text	Edited by	Edit
15210305	VEGF	VEGF	2.8	The potential role of the vascular endothelial growth gene (VEGF) VEGF as a risk/causitive risk causitive factor in ALS has been
15210305	VEGF	VEGF	2.8	VEGF induction occurs following the binding of hypoxia-inducible factors to the
15210305	VEGF	VEGF	2.8	VEGF coding region analysis has failed to identify mutations in ALS
15210305	VEGF	VEGF	2.8	of Swedish Belgian and English patients has revealed a specific VEGF haplotype in the promoter region which is associated with a
15210305	VEGF	VEGF	2.8	1.8 times greater risk of ALS and with lowered circulating VEGF levels in vivo 31 and 50
15210305	VEGF	VEGF	2.8	An increase of VEGF levels in serum but not in homogenates of spinal cord
15210305	VEGF	VEGF	2.8	during the course of the disease process generating a time-dependent VEGF tissue response 74
15691215	VEGF	VEGF	4.1	Mutations in the vascular endothelial growth factor gene (VEGF) VEGF also appear to be involved
15691215	VEGF	VEGF	4.1	Gene transfer of VEGF or glial cell-line derived neurotrophic factor anti-inflammatory COX-2 inhibitors and
16104843	VEGF	VEGF	10.4	Foremost among these is the VEGF (vascular vascular endothelial growth factor family and VEGFRs (VEGF VEGF
16104843	VEGF	VEGF	10.4	VEGF (vascular vascular endothelial growth factor family and VEGFRs (VEGF VEGF receptors
16104843	VEGF-A	VEGF-A	7.6	VEGF-A also referred to as VPF (vascular vascular permeability factor an
16104843	VPF	VPF	5.8	VEGF-A also referred to as VPF (vascular vascular permeability factor an important regulator of endothelial cell
16104843	VEGF-A	VEGF-A	7.6	VEGF-A is a dimeric glycoprotein essential for many angiogenic processes in
16104843	VEGF-A	VEGF-A	7.6	VEGF-A exhibits two major biological activities one is the capacity to
16104843	VEGF-A	VEGF-A	7.6	VEGF-A also promotes the survival and migration of endothelial cells
16104843	VEGF	VEGF	10.4	biological functions and the precise molecular mechanisms of the VEGF/VEGFR VEGF VEGFR system
16104843	VEGF	VEGF	10.4	the recent advances in the basic biology of the VEGF/VEGFR VEGF VEGFR system which give insight into many physiological and pathological
16104843	VEGF	VEGF	10.4	VEGF AND VEGF FAMILY PROTEINS
16104843	VEGF	VEGF	10.4	VEGF AND VEGF FAMILY PROTEINS
16104843	VEGF	VEGF	10.4	Currently the VEGF family includes VEGF-A PlGF (placenta placenta growth factor VEGF-B VEGF-C
16104843	VEGF-A	VEGF-A	7.6	Currently the VEGF family includes VEGF-A PlGF (placenta placenta growth factor VEGF-B VEGF-C VEGF-D VEGF-E and
16104843	VEGF	VEGF	10.4	factor VEGF-B VEGF-C VEGF-D VEGF-E and svVEGF (snake snake venom VEGF
16104843	VEGF-A	VEGF-A	7.6	VEGF-A
16104843	VEGF	VEGF	10.4	Structurally VEGF belongs to the VEGF/PDGF VEGF PDGF (platelet-derived platelet-derived growth factor
16104843	VEGF	VEGF	10.4	Structurally VEGF belongs to the VEGF/PDGF VEGF PDGF (platelet-derived platelet-derived growth factor supergene family
16104843	VEGF-A	VEGF-A	7.6	The human VEGF-A gene is organized into eight exons separated by seven introns
16104843	VEGF-A	VEGF-A	7.6	Human VEGF-A has at least nine subtypes due to the alternative splicing
16104843	VEGF	VEGF	10.4	subtypes due to the alternative splicing of a single gene VEGF 121 VEGF 145 VEGF 148 VEGF 162 VEGF 165 VEGF
16104843	VEGF	VEGF	10.4	to the alternative splicing of a single gene VEGF 121 VEGF 145 VEGF 148 VEGF 162 VEGF 165 VEGF 165 b
16104843	VEGF	VEGF	10.4	alternative splicing of a single gene VEGF 121 VEGF 145 VEGF 148 VEGF 162 VEGF 165 VEGF 165 b VEGF 183
16104843	VEGF	VEGF	10.4	of a single gene VEGF 121 VEGF 145 VEGF 148 VEGF 162 VEGF 165 VEGF 165 b VEGF 183 VEGF 189
16104843	VEGF	VEGF	10.4	single gene VEGF 121 VEGF 145 VEGF 148 VEGF 162 VEGF 165 VEGF 165 b VEGF 183 VEGF 189 and VEGF
16104843	VEGF	VEGF	10.4	VEGF 121 VEGF 145 VEGF 148 VEGF 162 VEGF 165 VEGF 165 b VEGF 183 VEGF 189 and VEGF 206 13
16104843	VEGF	VEGF	10.4	145 VEGF 148 VEGF 162 VEGF 165 VEGF 165 b VEGF 183 VEGF 189 and VEGF 206 13 14 ( Figure
16104843	VEGF	VEGF	10.4	148 VEGF 162 VEGF 165 VEGF 165 b VEGF 183 VEGF 189 and VEGF 206 13 14 ( Figure 1
16104843	VEGF	VEGF	10.4	VEGF 165 VEGF 165 b VEGF 183 VEGF 189 and VEGF 206 13 14 ( Figure 1
16104843	VEGF	VEGF	10.4	VEGF 165 b is an endogenous inhibitory form of VEGF which
16104843	VEGF	VEGF	10.4	VEGF 165 b is an endogenous inhibitory form of VEGF which binds VEGFR-2 with the same affinity as VEGF 165
16104843	VEGF	VEGF	10.4	of VEGF which binds VEGFR-2 with the same affinity as VEGF 165 but does not activate it or stimulate downstream signalling
16104843	VEGF	VEGF	10.4	VEGF is produced in endothelial cells macrophages activated T-cells and a
16104843	VEGF	VEGF	10.4	Although virtually nothing is known about how VEGF isoform levels are regulated most VEGF-producing cells appear to preferentially
16104843	VEGF	VEGF	10.4	levels are regulated most VEGF-producing cells appear to preferentially express VEGF 121 VEGF 165 and VEGF 189
16104843	VEGF	VEGF	10.4	regulated most VEGF-producing cells appear to preferentially express VEGF 121 VEGF 165 and VEGF 189
16104843	VEGF	VEGF	10.4	cells appear to preferentially express VEGF 121 VEGF 165 and VEGF 189
16104843	VEGF	VEGF	10.4	VEGF 165 the predominant isoform is secreted as an approx 46
16104843	VEGF	VEGF	10.4	In contrast VEGF 121 which lacks the residues encoded by exons 6 and
16104843	VEGF	VEGF	10.4	VEGF 189 which contains an additional sequence encoded by exon 6
16104843	VEGF	VEGF	10.4	VEGF 165 binds the coreceptors NRP-1 (neuropilin-1) neuropilin-1 20 and NRP-2
16104843	VEGF	VEGF	10.4	coreceptors NRP-1 (neuropilin-1) neuropilin-1 20 and NRP-2 (neuropilin-2), neuropilin-2 whereas VEGF 145 binds only NRP-2 21 ( Figure 2
16104843	VEGF	VEGF	10.4	Approx 50% of mice expressing exclusively the VEGF 120 isoform (murine murine VEGF is shorter by one amino
16104843	VEGF	VEGF	10.4	of mice expressing exclusively the VEGF 120 isoform (murine murine VEGF is shorter by one amino acid die within a few
16104843	VEGF	VEGF	10.4	VEGF mice also exhibit a specific decrease in capillary branch formation
16104843	VEGF	VEGF	10.4	retinal vascular outgrowth and patterning 24 suggesting that the heparin-binding VEGF isoforms provide spatially restricted stimulatory cues to initiate vascular branch
16104843	VEGF	VEGF	10.4	VEGF mice are normal and healthy and have a normal retinal
16104843	VEGF	VEGF	10.4	normal and healthy and have a normal retinal angiogenesis whereas VEGF mice display normal venular outgrowth but impaired arterial development in
16104843	VEGF	VEGF	10.4	These findings suggest that the various VEGF isoforms play distinct roles in vascular patterning and arterial development
16104843	VEGF	VEGF	10.4	distinct roles in vascular patterning and arterial development although the VEGF 164 isoform plays a central role in vascular development
16104843	VEGF	VEGF	10.4	Gene expression of VEGF is regulated by a variety of stimuli such as hypoxia
16104843	VEGF	VEGF	10.4	all of the stimuli responsible for the up-regulation of the VEGF gene are quite interesting hypoxia has been of particular interest
16104843	VEGF	VEGF	10.4	a HRE (hypoxia hypoxia response element -driven transcription of the VEGF gene 28
16104843	VEGF-A	VEGF-A	7.6	a protein accumulates under normoxic conditions and the transcription of VEGF-A is increased 29
16104843	VEGF	VEGF	10.4	VEGF is also regulated at the level of mRNA stability
16104843	VEGF	VEGF	10.4	The 5_amp_#180;- and 3_amp_#180 -UTRs (untranslated untranslated regions of the VEGF gene confer increased mRNA stability during hypoxia
16104843	VEGF	VEGF	10.4	protein-interacting protein 2 have been identified as crucial proteins for VEGF mRNA stabilization 30 31
16104843	VEGF	VEGF	10.4	Furthermore VEGF expression can be regulated at the translational level
16104843	VEGF	VEGF	10.4	It has been shown that the 5_amp_#180 -UTR of VEGF mRNA contains two functional internal ribosome entry sites that maintain
16104843	VEGF	VEGF	10.4	that maintain efficient cap-independent translation and ensure efficient production of VEGF even under unfavourable stress conditions such as hypoxia 32
16104843	VEGF-A	VEGF-A	7.6	PlGF-1 has shown that this protein is structurally similar to VEGF-A 40
16104843	VEGF-A	VEGF-A	7.6	Furthermore despite this moderate sequence conservation PlGF and VEGF-A bind to the same binding interface of VEGFR-1 in a
16104843	VEGF-A	VEGF-A	7.6	However recent studies have reported that unlike in VEGF-A N-glycosylation in PlGF plays an important role in VEGFR-1 binding
16104843	VEGF	VEGF	10.4	contains a region sharing approx 30% amino acid identity with VEGF 165 however it is more closely related to VEGF-D by
16104843	VEGF	VEGF	10.4	N- and C-terminal extensions that are not found in other VEGF family members 49 ( Figure 1
16104843	VEGF-A	VEGF-A	7.6	a member of the VEGFR family that does not bind VEGF-A as well as VEGFR-2 and are mitogenic for cultured endothelial
16104843	VEGF	VEGF	10.4	a preproprotein with long N- and C-terminal propeptides flanking the VEGF homology domain
16104843	VEGF	VEGF	10.4	Homologues of VEGF have also been identified in the genome of the parapoxvirus
16104843	VEGF-A	VEGF-A-like	5.8	parapoxvirus Orf virus 54 and have been shown to have VEGF-A-like activities
16104843	VEGF	VEGF	10.4	for a group of these proteins including VEGF-E NZ-2 (VEGF VEGF from Orf virus strain NZ-2 55 VEGF-E NZ-7 (VEGF VEGF
16104843	VEGF	VEGF	10.4	VEGF from Orf virus strain NZ-2 55 VEGF-E NZ-7 (VEGF VEGF from Orf virus strain NZ-7 56 VEGF-E NZ-10 (VEGF VEGF
16104843	VEGF	VEGF	10.4	VEGF from Orf virus strain NZ-7 56 VEGF-E NZ-10 (VEGF VEGF from Orf virus strain NZ-10 57 VEGF-E D1701 (VEGF VEGF
16104843	VEGF	VEGF	10.4	VEGF from Orf virus strain NZ-10 57 VEGF-E D1701 (VEGF VEGF from Orf virus strain D1701 58 and VEGF-E VR634 (VEGF
16104843	VEGF	VEGF	10.4	from Orf virus strain D1701 58 and VEGF-E VR634 (VEGF VEGF from Pseudocowpox virus strain VR634 57
16104843	VEGF	VEGF	10.4	VEGF-E seems to be as potent as VEGF 165 at stimulating endothelial cell proliferation despite lacking a heparin-binding
16104843	VEGF	VEGF	10.4	Recently VEGF family proteins have been identified in snake venom including svVEGF
16104843	VEGF	VEGFs	5.8	et al 61 have shown that snakes utilize these venom-specific VEGFs in addition to VEGF-A svVEGFs function as dimers and each
16104843	VEGF-A	VEGF-A	7.6	shown that snakes utilize these venom-specific VEGFs in addition to VEGF-A svVEGFs function as dimers and each chain comprises approx 110-122
16104843	VEGF	VEGF	10.4	The cysteine knot motif a characteristic of the VEGF family of proteins is completely conserved in svVEGFs and the
16104843	VEGF	VEGF	10.4	completely conserved in svVEGFs and the sequence identity with human VEGF 165 is approx 50% ( Figure 1
16104843	VEGF	VEGF	10.4	VEGFR-1 but binds VEGFR-2 with high affinity as well as VEGF 165 64
16104843	VEGF	VEGF	10.4	with high affinity and VEGFR-2 with low affinity compared with VEGF 165 leading to a strong enhancement of vascular permeability but
16104843	VEGF-A	VEGF-A	7.6	VEGFR-1 is a 180 kDa high-affinity receptor for VEGF-A VEGF-B PlGF and Tf svVEGF
16104843	VEGF-A	VEGF-A	7.6	Ig domain of VEGFR-1 is the major binding site for VEGF-A and PlGF 16 41 67
16104843	VEGF-A	VEGF-A	7.6	VEGFR-1 binds VEGF-A with at least 10-fold higher affinity than VEGFR-2 ( K
16104843	VEGF-A	VEGF-A	7.6	HUVECs (human human umbilical vein endothelial cells in response to VEGF-A indicating the involvement of VEGFR-1 in endothelial cell migration 68
16104843	VEGF-A	VEGF-A	7.6	a HUVEC cDNA library 16 sVEGFR-1 (soluble soluble VEGFR-1 inhibits VEGF-A activity by sequestering VEGF-A from signalling receptors and by forming
16104843	VEGF-A	VEGF-A	7.6	16 sVEGFR-1 (soluble soluble VEGFR-1 inhibits VEGF-A activity by sequestering VEGF-A from signalling receptors and by forming non-signalling heterodimers with VEGFR-2
16104843	VEGF	VEGF	10.4	with pre-eclampsia are associated with decreased circulating levels of free VEGF and PlGF resulting in general endothelial dysfunction 73
16104843	VEGF-A	VEGF-A	7.6	VEGFR-2 is a 200-230 kDa high-affinity receptor for VEGF-A ( K d =75-760 pM VEGF-E and svVEGFs as well
16104843	VEGF-A	VEGF-A	7.6	The binding site for VEGF-A has been mapped to the second and third Ig domains
16104843	VEGF-A	VEGF-A	7.6	Tyrosine phosphorylation sites in human VEGFR-2 bound to VEGF-A are Tyr and Tyr in the kinase-insert domain Tyr and
16104843	VEGF-A	VEGF-A-dependent	5.8	Among them Tyr and Tyr are the two major VEGF-A-dependent autophosphorylation sites 76
16104843	VEGF-A	VEGF-A	7.6	major mediator of the mitogenic angiogenic and permeability-enhancing effects of VEGF-A
16104843	VEGF-A	VEGF-A	7.6	al 84 have reported that the activation of VEGFR-2 by VEGF-A results in the PI3K/Akt-dependent PI3K Akt-dependent activation of several integrins
16104843	VEGF	VEGF-mediated	5.8	(soluble soluble VEGFR-2 may have regulatory consequences with respect to VEGF-mediated angiogenesis
16104843	VEGF-A	VEGF-A	7.6	guidance 90 and subsequently found as an isoform-specific receptor for VEGF-A 20
16104843	VEGF	VEGF	10.4	NRP-1 is able to bind VEGF 165 VEGF-B PlGF-2 and some VEGF-E variants whereas NRP-2 can
16104843	VEGF	VEGF	10.4	VEGF-B PlGF-2 and some VEGF-E variants whereas NRP-2 can bind VEGF 145 VEGF 165 PlGF-2 and VEGF-C
16104843	VEGF	VEGF	10.4	and some VEGF-E variants whereas NRP-2 can bind VEGF 145 VEGF 165 PlGF-2 and VEGF-C
16104843	VEGF	VEGF	10.4	the independent transduction of biological signals subsequent to semaphorin or VEGF binding
16104843	VEGF	VEGF	10.4	The VEGF 165 -induced proliferation and migration of cells that express VEGFR-2
16104843	VEGF	VEGF	10.4	as an enhancer of VEGFR-2 activity in the presence of VEGF 165
16104843	VEGF	VEGF	10.4	VEGF/VEGFR VEGF VEGFR SYSTEM IN PHYSIOLOGICAL AND PATHOLOGICAL CONDITIONS
16104843	VEGF	VEGF	10.4	The loss of a single VEGF allele is lethal in the mouse embryo between days 11
16104843	VEGF	VEGF	10.4	VEGF embryos exhibit significant defects in the vasculature of several organs
16104843	VEGF-A	VEGF-A	7.6	In addition a 2- to 3-fold overexpression of VEGF-A from its endogenous locus results in severe abnormalities in heart
16104843	VEGF-A	VEGF-A	7.6	These results demonstrate the importance of tightly regulating VEGF-A expression during embryonic development
16104843	VEGF-A	VEGF-A-dependent	5.8	76 have shown that Tyr and Tyr are two major VEGF-A-dependent autophosphorylation sites in VEGFR-2
16104843	VEGF	VEGF-dependent	5.8	However only autophosphorylation of Tyr is crucial for VEGF-dependent endothelial cell proliferation via the PLC-g /PKC/Raf/MEK PKC Raf MEK
16104843	VEGF-A	VEGF-A	7.6	actin remodelling in stress fibres in endothelial cells exposed to VEGF-A 106
16104843	VEGF-A	VEGF-A-induced	5.8	(S6 S6 kinase pathway by VEGFR-2 is also involved in VEGF-A-induced endothelial cell proliferation 107 ( Figure 2
16104843	VEGF	VEGF-induced	5.8	In addition recent studies have revealed various downstream mediators of VEGF-induced angiogenic signalling such as diacylglycerol kinase a 109 SRF (serum
16104843	VEGF	VEGF-induced	5.8	using DNA microarrays have reported possible endogenous feedback inhibitors for VEGF-induced angiogenesis
16104843	VEGF	VEGF	10.4	Down syndrome critical region protein 1 are significantly induced by VEGF in endothelial cells 113 114
16104843	VEGF-A	VEGF-A	7.6	VEGF-A is known to increase the vascular permeability of microvessels to
16104843	VEGF-A	VEGF-A	7.6	VEGF-A significantly accumulates in malignant ascites 116 and pleural effusion 117
16104843	VEGF-A	VEGF-A	7.6	Consistent with a role in the regulation of vascular permeability VEGF-A induces endothelial fenestration in some vascular beds and in cultured
16104843	VEGF-A	VEGF-A	7.6	VEGF-A increases vascular permeability in mesenteric microvessels by activation of VEGFR-2
16104843	VEGF	VEGF-dependent	5.8	in specific Src family kinases has demonstrated no decrease in VEGF-dependent neovascularization but a complete ablation of vascular permeability in Src
16104843	VEGF	VEGF-mediated	5.8	b -catenin with the same kinetics with which it prevents VEGF-mediated vascular permeability and oedema 120
16104843	VEGF	VEGF-induced	5.8	activity of specific Src family kinases is essential for the VEGF-induced enhancement of vascular permeability through the disruption of the VEGFR-2/cadherin/catenin
16104843	VEGF-A	VEGF-A	7.6	VEGF-A can induce production of NO and endogenous NO can increase
16104843	VEGF	VEGF-induced	5.8	synthase eNOS (endothelial endothelial NOS plays a predominant role in VEGF-induced angiogenesis and vascular permeability 122
16104843	VEGF	VEGF-induced	5.8	126 has shown that inhibition of p38 MAPK activity abrogated VEGF-induced vascular permeability in vivo and in vitro suggesting the involvement
16104843	VEGF-A	VEGF-A	7.6	Numerous studies have established VEGF-A as a key angiogenic player in cancer
16104843	VEGF-A	VEGF-A	7.6	VEGF-A is expressed in most tumours and its expression correlates with
16104843	VEGF-A	VEGF-A	7.6	tumour cells tumour-associated stroma is also an important source of VEGF-A 127
16104843	VEGF-A	VEGF-A	7.6	The expression of VEGF-A mRNA is highest in hypoxic tumour cells adjacent to necrotic
16104843	VEGF-A	VEGF-A	7.6	adjacent to necrotic areas 16 indicating that the induction of VEGF-A by hypoxia in growing tumours can change the balance of
16104843	VEGF	VEGF	10.4	Consistent with this hypothesis capturing of VEGF or blocking of its signalling receptor VEGFR-2 by a VEGFR
16104843	VEGF	VEGF-driven	5.8	regulates inter- and intra-molecular cross-talk between VEGFR-1 and VEGFR-2 amplifying VEGF-driven angiogenesis through VEGFR-2
16104843	VEGF	VEGF	10.4	Several studies also describe the role of VEGF in carcinogenesis 132
16104843	VEGF-A	VEGF-A	7.6	VEGF-A and VEGFRs are constitutively expressed in the islet vasculature before
16104843	VEGF-A	VEGF-A	7.6	the initiation of angiogenesis (angiogenic angiogenic switch 133 however when VEGF-A is absent from islet b -cells of Rip1-Tag2 mice both
16104843	VEGF-A	VEGF-A	7.6	well as tumour growth are severely disrupted 134 indicating that VEGF-A plays a critical role in angiogenic switching and carcinogenesis
16104843	VEGF-A	VEGF-A	7.6	a component of the angiogenic switch as this proteinase makes VEGF-A available for the interaction with its receptors by releasing sequestered
16104843	VEGF-A	VEGF-A	7.6	available for the interaction with its receptors by releasing sequestered VEGF-A
16104843	VEGF-A	VEGF-A	7.6	VEGF-A impairs the endothelial barrier by disrupting a VE-cadherin/ VE-cadherin b
16104843	VEGF-A	VEGF-A	7.6	VEGF-A also induces the disruption of hepatocellular tight junctions which may
16104843	VEGF	VEGF	10.4	Besides bevacizumab many other VEGF inhibitors are being pursued clinically
16104843	VEGF	VEGF	10.4	VEGF acts as a pro-inflammatory cytokine by increasing the permeability of
16104843	VEGF	VEGF	10.4	VEGF is strongly expressed by epidermal keratinocytes in wound healing and
16104843	VEGF-A	VEGF-A	7.6	Transgenic mice that overexpress VEGF-A specifically in the epidermis exhibit an increased density of tortuous
16104843	VEGF-A	VEGF-A	7.6	adhesion in postcapillary skin venules suggesting that enhanced expression of VEGF-A in epidermal keratinocytes is sufficient to develop psoriasis-like inflammatory skin
16104843	VEGF-A	VEGF-A	7.6	Moreover heterozygous VEGF-A transgenic mice which do not spontaneously develop inflammatory skin lesions
16104843	VEGF-A	VEGF-A	7.6	Local production of VEGF-A in arthritic synovial tissue has been documented 16 and appears
16104843	VEGF-A	VEGF-A	7.6	Subsequently VEGF-A has been shown to be important in the pathogenesis of
16104843	VEGF-A	VEGF-A	7.6	Exaggerated levels of VEGF-A have been detected in tissues and biological samples from people
16104843	VEGF	VEGF	10.4	VEGF has been postulated to contribute to asthmatic tissue oedema through
16104843	VEGF	VEGF	10.4	A recent study using lung-targeted VEGF 165 transgenic mice has revealed a novel function of VEGF-A
16104843	VEGF-A	VEGF-A	7.6	VEGF 165 transgenic mice has revealed a novel function of VEGF-A in allergic responses
16104843	VEGF-A	VEGF-A	7.6	In these mice VEGF-A induces asthma-like inflammation airway and vascular remodelling and airway hyper-responsiveness
16104843	VEGF-A	VEGF-A	7.6	VEGF-A also enhances respiratory sensitization to antigen as well as T
16104843	VEGF-A	VEGF-A	7.6	Thus VEGF-A has a critical role in pulmonary T H 2 inflammation
16104843	VEGF-A	VEGF-A	7.6	Other studies have provided evidence for a role for VEGF-A as a pro-inflammatory mediator in allograft rejection 152 and neointimal
16104843	VEGF-A	VEGF-A	7.6	VEGF-A mRNA expression not normally found in the adult mouse brain
16104843	VEGF-A	VEGF-A	7.6	adult mouse brain is up-regulated after cerebral ischaemia and elevated VEGF-A levels can be detected as early as 3 h after
16104843	VEGF-A	VEGF-A	7.6	Previous studies have demonstrated that the antagonism of VEGF-A results in reduced oedema and tissue damage after ischaemia implicating
16104843	VEGF-A	VEGF-A	7.6	results in reduced oedema and tissue damage after ischaemia implicating VEGF-A in the pathophysiology of stroke 155
16104843	VEGF-A	VEGF-A-induced	5.8	al 156 have reported that Src mice are resistant to VEGF-A-induced vascular permeability and show decreased infarct volumes after stroke
16104843	VEGF-A	VEGF-A	7.6	permeability protecting wild-type mice from ischaemia-induced brain damage without influencing VEGF-A expression
16104843	VEGF-A	VEGF-A	7.6	Sun et al 157 have reported that intracerebroventricular administration of VEGF-A reduces infarct size improves neurological performance and enhances the delayed
16104843	VEGF-A	VEGF-A	7.6	These conflicting results appear to reflect dual roles of VEGF-A in stroke neuroprotective and pro-inflammatory effects
16104843	VEGF-A	VEGF-A	7.6	through the internal carotid artery low and intermediate doses of VEGF-A significantly promote neuroprotection of the ischaemic brain whereas a high
16104843	VEGF-A	VEGF-A	7.6	neuroprotection of the ischaemic brain whereas a high dose of VEGF-A offers no neuroprotection to the ischaemic brain or the damaged
16104843	VEGF-A	VEGF-A	7.6	Further studies are required for the therapeutic application of VEGF-A against stroke
16104843	VEGF	VEGF	10.4	Extensive evidence has suggested a causal role of VEGF in several diseases of the human eye in which neovascularization
16104843	VEGF	VEGF	10.4	VEGF levels are increased in the vitreous and retina of patients
16104843	VEGF	VEGF	10.4	Subsequent studies using various VEGF inhibitors have confirmed that VEGF plays a central role in
16104843	VEGF	VEGF	10.4	Subsequent studies using various VEGF inhibitors have confirmed that VEGF plays a central role in ischaemia-induced intraocular neovascularization 159
16104843	VEGF	VEGF	10.4	161 have reported that deletion of the HRE in the VEGF promoter reduces hypoxic VEGF expression in the spinal cord and
16104843	VEGF	VEGF	10.4	deletion of the HRE in the VEGF promoter reduces hypoxic VEGF expression in the spinal cord and causes adult-onset progressive motor
16104843	VEGF	VEGF	10.4	VEGF 165 promotes survival of motor neurons during hypoxia through binding
16104843	VEGF-A	VEGF-A	7.6	A subsequent study has revealed that VEGF-A is a modifier associated with motor neuron degeneration in human
16104843	VEGF-A	VEGF-A	7.6	VEGF-A treatment increases the life expectancy of ALS mice without causing
16104843	VEGF-A	VEGF-A	7.6	mice without causing toxic side effects 163 164 indicating that VEGF-A has neuroprotective effects on motor neurons and treatment with VEGF-A
16104843	VEGF-A	VEGF-A	7.6	VEGF-A has neuroprotective effects on motor neurons and treatment with VEGF-A could be one of the most effective therapies for ALS
16104843	VEGF-A	VEGF-A	7.6	VEGF-A has no direct mitogenic effect on hepatocytes
16104843	VEGF	VEGF	10.4	VEGF was originally described as a specific angiogenic and permeability-inducing factor
16104843	VEGF	VEGF	10.4	emerging evidence has revealed that the role of the VEGF/VEGFR VEGF VEGFR system extends far beyond previous expectations
16104843	VEGF	VEGF	10.4	First a wide variety of VEGF family proteins and numerous splicing variants have been identified and
16104843	VEGF	VEGF	10.4	VEGF family proteins have been utilized even in snake venoms and
16104843	VEGF	VEGF	10.4	Thirdly it has been shown that the VEGF/VEGFR VEGF VEGFR system has multiple functions such as the induction of
16104843	VEGF	VEGF	10.4	VEGF is also important for memory and learning 167
16104843	VEGF	VEGF	10.4	other molecules have been found to associate with the VEGF/VEGFR VEGF VEGFR system
16104843	VEGF	VEGF	10.4	are required to achieve a comprehensive understanding of the VEGF/VEGFR VEGF VEGFR system however the recent progress in the molecular and
16104843	VEGF	VEGF	10.4	angiogenesis inflammation signal transduction tumour vascular endothelial growth factor (VEGF), VEGF vascular permeability
16104843	VEGF	VEGF	10.4	antigen T H 2 T-helper type 2 UTR untranslated region VEGF vascular endothelial growth factor VEGFR VEGF receptor sVEGFR-1 soluble VEGFR-1
16104843	VEGF	VEGF	10.4	2 UTR untranslated region VEGF vascular endothelial growth factor VEGFR VEGF receptor sVEGFR-1 soluble VEGFR-1 svVEGF snake venom VEGF Tf svVEGF
16104843	VEGF	VEGF	10.4	factor VEGFR VEGF receptor sVEGFR-1 soluble VEGFR-1 svVEGF snake venom VEGF Tf svVEGF Trimeresurus flavoviridis svVEGF VPF vascular permeability factor
16104843	VPF	VPF	5.8	VEGFR-1 svVEGF snake venom VEGF Tf svVEGF Trimeresurus flavoviridis svVEGF VPF vascular permeability factor
16104843	VEGF	VEGF	10.4	The VEGF (vascular vascular endothelial growth factor family and its receptors are
16104843	VEGF	VEGF	10.4	Currently the VEGF family consists of VEGF-A PlGF (placenta placenta growth factor VEGF-B
16104843	VEGF-A	VEGF-A	7.6	Currently the VEGF family consists of VEGF-A PlGF (placenta placenta growth factor VEGF-B VEGF-C VEGF-D VEGF-E and
16104843	VEGF	VEGF	10.4	placenta growth factor VEGF-B VEGF-C VEGF-D VEGF-E and snake venom VEGF
16104843	VEGF-A	VEGF-A	7.6	VEGF-A has at least nine subtypes due to the alternative splicing
16104843	VEGF	VEGF	10.4	Although the VEGF 165 isoform plays a central role in vascular development recent
16104843	VEGF	VEGF	10.4	role in vascular development recent studies have demonstrated that each VEGF isoform plays distinct roles in vascular patterning and arterial development
16104843	VEGF-A	VEGF-A	7.6	VEGF-A binds to and activates two tyrosine kinase receptors VEGFR (VEGF
16104843	VEGF	VEGF	10.4	binds to and activates two tyrosine kinase receptors VEGFR (VEGF VEGF receptor -1 and VEGFR-2
16104843	VEGF-A	VEGF-A	7.6	In solid tumours VEGF-A and its receptor are involved in carcinogenesis invasion and distant
16104843	VEGF-A	VEGF-A	7.6	VEGF-A also has a neuroprotective effect on hypoxic motor neurons and
16104843	VEGF	VEGF	10.4	progress in the molecular and biological understanding of the VEGF/VEGFR VEGF VEGFR system provides us with novel and promising therapeutic strategies
16380619	VEGF	VEGF	3.3	and growth factors such as vascular endothelial growth factor (VEGF) VEGF thought to play a role in the pathophysiology of sporadic
16380619	VEGF	VEGF	3.3	Expression of the VEGF gene is mainly stimulated by hypoxia through the binding of
16380619	VEGF	VEGF	3.3	In CNS VEGF is mostly synthesized by endothelial cells and microglia
16380619	VEGF	VEGF	3.3	angiogenic properties and reciprocal interactions between COX-2/PGE-2 COX-2 PGE-2 and VEGF are described
16380619	VEGF	VEGF	3.3	ALS because they can block the natural upregulation loop of VEGF during hypoxemia
17015226	VEGF	VEGF	4.3	Mutations in genes encoding angiogenin ( ANG and VEGF and sequence variants in neurofilament genes have also been reported
17015226	VEGF	VEGF	4.3	since only ALS1 ALS3 ALS6 ALS7 mutations in angiogenin and VEGF and a small proportion of incidences of ALS8 represent the
17015226	VEGF	VEGF	4.3	Vascular Endothelial Growth Factor (VEGF) VEGF
17015226	VEGF	VEGF	4.3	Vascular endothelial growth factor (VEGF), VEGF an established regulator of developmental hypoxia-induced and tumor-induced angiogenesis gained
17015226	VEGF	VEGF	4.3	of the hypoxia response element (HRE) HRE in the murine VEGF promoter resulted in ALS-like disease in mice ( Oosthuyse et_amp_#xa0
17015226	VEGF	VEGF	4.3	VEGF is widely expressed throughout the central nervous system (CNS) CNS
17015226	VEGF	VEGF	4.3	Screening of ALS patient DNAs in promoter regions of the VEGF gene including the HRE and regions known to correlate with
17015226	VEGF	VEGF	4.3	the HRE and regions known to correlate with downregulation of VEGF synthesis found no link between HRE variants and disease (
17015226	VEGF	VEGF	4.3	Whether angiogenin is endowed with neurotrophic properties like VEGF in addition to its angiogenic activity is not yet established
17015226	VEGF	VEGF	4.3	SOD1 and VAPB or expressed in multiple cells types ( VEGF and ANG
17015226	VEGF	VEGF	4.3	With the potential that variants in the VEGF gene contribute to some examples of ALS ( Table 1
17015226	VEGF	VEGF	4.3	ALS ( Table 1 delivery of an integrating lentivirus encoding VEGF (and and pseudocoated so as to be retrogradely transported extended
17015226	VEGF	VEGF	4.3	So too did continuous ICV infusion of recombinant VEGF protein into the CSF ( Figure_amp_#xa0 4 B disease onset
17015226	VEGF	VEGF	4.3	This ICV delivery of VEGF was especially effective in slowing forelimb paralysis suggestive of a
17015226	VEGF	VEGF	4.3	in slowing forelimb paralysis suggestive of a higher concentration of VEGF closer to the site of infusion
17015226	VEGF	VEGF	4.3	A modest benefit was seen even when VEGF treatment was initiated after symptomatic onset
17015226	VEGF	VEGF	4.3	Unresolved is which cells are targeted by this VEGF
17015226	VEGF	VEGF	4.3	Weekly intraperitoneal injection of VEGF also has been reported to slow disease in hSOD1 G93A
17582695	VEGF	VEGF	2.8	influencing vessel plasticity along with vascular endothelial growth factor (VEGF) VEGF 22
17582695	VEGF	VEGF	2.8	Serum VEGF is higher in ALS in human samples than controls 23
17582695	VEGF	VEGF	2.8	samples than controls 23 as it is in MS where VEGF shows a correlation with length of spinal cord lesions 24
17582695	VEGF	VEGF	2.8	High erythropoietin and low VEGF in CSF from hypoxemic ALS patients suggest an abnormal response
15691215	vascular endothelial growth factor	vascular endothelial growth factor	1.0	mutations in the vascular endothelial growth factor gene vegf also appear to be involved.
16104843	vascular endothelial growth factor	vascular endothelial growth factor	1.0	foremost among these is the vegf vascular endothelial growth factor family and vegfrs vegf receptors .
16104843	vegf a	vegf a	1.0	vegf a also referred to as vpf vascular permeability factor an important regulator of endothelial cell physiology was identified approx. 15 years ago [ 1 2 ] and has been recognized as the major growth fact
16104843	vascular permeability factor	vascular permeability factor	1.0	vegf a also referred to as vpf vascular permeability factor an important regulator of endothelial cell physiology was identified approx. 15 years ago [ 1 2 ] and has been recognized as the major growth factor that is relatively specific for endothelial cells.
16104843	vegf a	vegf a	1.0	vegf a is a dimeric glycoprotein essential for many angiogenic processes in normal and abnormal states such as tumour vascularization mainly by interacting with two tyrosine kinase receptors vegfr 1 [also k
16104843	vegf a	vegf a	1.0	vegf a exhibits two major biological activities: one is the capacity to stimulate vascular endothelial cell proliferation [ 1 6 7 ] and the other is the ability to increase vascular permeability [ 2 8 ].
16104843	vegf a	vegf a	1.0	vegf a also promotes the survival and migration of endothelial cells.
16104843	vegf a	vegf a	1.0	currently the vegf family includes vegf a plgf placenta growth factor vegf b vegf c vegf d vegf e and svvegf snake venom vegf .
16104843	vegf a	vegf a	1.0	vegf a
16104843	vegf a	vegf a	1.0	the human vegf a gene is organized into eight exons separated by seven introns [ 10 11 ] and is located at 6p21.3 [ 12 ].
16104843	vegf a	vegf a	1.0	human vegf a has at least nine subtypes due to the alternative splicing of a single gene: vegf 121 vegf 145 vegf 148 vegf 162 vegf 165 vegf 165 b vegf 183 vegf 189 and vegf 206 [ 13 14 ] figure 1 .
16104843	vegf a	vegf a	1.0	consequently hif 1 a protein accumulates under normoxic conditions and the transcription of vegf a is increased [ 29 ].
16104843	vegf a	vegf a	1.0	the crystal structure of human plgf 1 has shown that this protein is structurally similar to vegf a [ 40 ].
16104843	vegf a	vegf a	1.0	furthermore despite this moderate sequence conservation plgf and vegf a bind to the same binding interface of vegfr 1 in a very similar fashion [ 41 ].
16104843	vegf a	vegf a	1.0	however recent studies have reported that unlike in vegf a n glycosylation in plgf plays an important role in vegfr 1 binding [ 42 ].
16104843	vegf a	vegf a	1.0	both vegf c and vegf d bind and activate vegfr 3 flt 4; a member of the vegfr family that does not bind vegf a as well as vegfr 2 and are mitogenic for cultured endothelial cells.
16104843	vegf a	vegf a	1.0	homologues of vegf have also been identified in the genome of the parapoxvirus orf virus [ 54 ] and have been shown to have vegf a like activities.
16104843	vegf a	vegf a	1.0	takahashi et al. [ 61 ] have shown that snakes utilize these venom specific vegfs in addition to vegf a. svvegfs function as dimers and each chain comprises approx. 110 122 amino acid residues.
16104843	vegf a	vegf a	1.0	vegfr 1 is a 180 kda high affinity receptor for vegf a vegf b plgf and tf svvegf.
16104843	vegf a	vegf a	1.0	the second ig domain of vegfr 1 is the major binding site for vegf a and plgf [ 16 41 67 ].
16104843	vegf a	vegf a	1.0	vegfr 1 binds vegf a with at least 10 fold higher affinity than vegfr 2 k d =10 30 pm [ 16 ]; however ligand binding results in a maximal 2 fold increase in kinase activity.
16104843	vegf a	vegf a	1.0	vegfr 1 blocking antibodies prevent the migration but not proliferation of huvecs human umbilical vein endothelial cells in response to vegf a indicating the involvement of vegfr 1 in endothelial cell migration [ 68 ].
16104843	vegf a	vegf a	1.0	iced form of vegfr 1 that encodes a soluble truncated form of the receptor containing only the first six ig domains has been cloned from a huvec cdna library [ 16 ]. svegfr 1 soluble vegfr 1 inhibits vegf a activity by sequestering vegf a from signalling receptors and by forming non signalling heterodimers with vegfr 2 [ 69 ].
16104843	vegf a	vegf a	1.0	activity by sequestering vegf a from signalling receptors and by forming non signalling heterodimers with vegfr 2 [ 69 ].
16104843	vegf a	vegf a	1.0	vegfr 2 is a 200 230 kda high affinity receptor for vegf a k d =75 760 pm vegf e and svvegfs as well as the processed form of vegf c and vegf d.
16104843	vegf a	vegf a	1.0	the binding site for vegf a has been mapped to the second and third ig domains [ 74 ].
16104843	vegf a	vegf a	1.0	tyrosine phosphorylation sites in human vegfr 2 bound to vegf a are tyr and tyr in the kinase insert domain tyr and tyr in the kinase domain and tyr and tyr in the c terminal tail.
16104843	vegf a	vegf a	1.0	among them tyr and tyr are the two major vegf a dependent autophosphorylation sites [ 76 ].
16104843	vegf a	vegf a	1.0	vegfr 2 is the major mediator of the mitogenic angiogenic and permeability enhancing effects of vegf a.
16104843	vegf a	vegf a	1.0	byzova et al. [ 84 ] have reported that the activation of vegfr 2 by vegf a results in the pi3k/akt dependent activation of several integrins leading to enhanced cell adhesion and migration.
16104843	vegf a	vegf a	1.0	nrp 1 is a 130 140 kda cell surface glycoprotein first identified as a semaphorin receptor involved in neuronal guidance [ 90 ] and subsequently found as an isoform specific receptor for vegf a [ 20 ].
16104843	vegf a	vegf a	1.0	in addition a 2 to 3 fold overexpression of vegf a from its endogenous locus results in severe abnormalities in heart development and lethality at embryonic days 12.5 and 14 [ 100 ].
16104843	vegf a	vegf a	1.0	these results demonstrate the importance of tightly regulating vegf a expression during embryonic development.
16104843	vegf a	vegf a	1.0	takahashi et al. [ 76 ] have shown that tyr and tyr are two major vegf a dependent autophosphorylation sites in vegfr 2.
16104843	vegf a	vegf a	1.0	sphorylation of tyr appears to be required to trigger the sequential activation of cdc42 and p38 mapk and to drive p38 mapk mediated actin remodelling in stress fibres in endothelial cells exposed to vegf a [ 106 ].
16104843	vegf a	vegf a	1.0	the activation of the pi3k/p70 s6k s6 kinase pathway by vegfr 2 is also involved in vegf a induced endothelial cell proliferation [ 107 ] figure 2 .
16104843	vegf a	vegf a	1.0	vegf a is known to increase the vascular permeability of microvessels to circulating macromolecules [ 14 ].
16104843	vegf a	vegf a	1.0	vegf a significantly accumulates in malignant ascites [ 116 ] and pleural effusion [ 117 ] suggesting that it plays a fundamental role in the accumulation of malignant fluid through the enhancement of vascu
16104843	vegf a	vegf a	1.0	consistent with a role in the regulation of vascular permeability vegf a induces endothelial fenestration in some vascular beds and in cultured adrenal endothelial cells the extravasation of ferritin by way of the vvo vesiculo vacuolar organelle [ 14 ] and disorganization
16104843	vegf a	vegf a	1.0	vegf a increases vascular permeability in mesenteric microvessels by activation of vegfr 2 on endothelial cells and subsequent activation of plc.
16104843	vegf a	vegf a	1.0	vegf a can induce production of no and endogenous no can increase vascular permeability [ 121 ].
16104843	vegf a	vegf a	1.0	numerous studies have established vegf a as a key angiogenic player in cancer.
16104843	vegf a	vegf a	1.0	vegf a is expressed in most tumours and its expression correlates with tumour progression.
16104843	vegf a	vegf a	1.0	in addition to tumour cells tumour associated stroma is also an important source of vegf a [ 127 ].
16104843	vegf a	vegf a	1.0	the expression of vegf a mrna is highest in hypoxic tumour cells adjacent to necrotic areas [ 16 ] indicating that the induction of vegf a by hypoxia in growing tumours can change the balance of inhibitors and activators of angiogenesis leading to the growth of new blood vessels into tumour.
16104843	vegf a	vegf a	1.0	vegf a and vegfrs are constitutively expressed in the islet vasculature before and after the initiation of angiogenesis angiogenic switch [ 133 ]; however when vegf a is absent from islet b cells of rip1 tag2 mice both angiogenic switching and carcinogenesis as well as tumour growth are severely disrupted [ 134 ] indicating that vegf a plays a critical role in ang
16104843	vegf a	vegf a	1.0	is absent from islet b cells of rip1 tag2 mice both angiogenic switching and carcinogenesis as well as tumour growth are severely disrupted [ 134 ] indicating that vegf a plays a critical role in angiogenic switching and carcinogenesis.
16104843	vegf a	vegf a	1.0	bergers et al. [ 135 ] have revealed that mmp matrix metalloproteinase 9 is also a component of the angiogenic switch as this proteinase makes vegf a available for the interaction with its receptors by releasing sequestered vegf a.
16104843	vegf a	vegf a	1.0	available for the interaction with its receptors by releasing sequestered vegf a.
16104843	vegf a	vegf a	1.0	vegf a impairs the endothelial barrier by disrupting a ve cadherin/ b catenin complex via the activation of src and facilitates tumour cell extravasation and metastasis [ 136 ].
16104843	vegf a	vegf a	1.0	vegf a also induces the disruption of hepatocellular tight junctions which may promote tumour invasion [ 137 ].
16104843	vegf a	vegf a	1.0	transgenic mice that overexpress vegf a specifically in the epidermis exhibit an increased density of tortuous cutaneous blood capillaries as well as highly increased leucocyte rolling and adhesion in postcapillary skin venules suggesting
16104843	vegf a	vegf a	1.0	is exhibit an increased density of tortuous cutaneous blood capillaries as well as highly increased leucocyte rolling and adhesion in postcapillary skin venules suggesting that enhanced expression of vegf a in epidermal keratinocytes is sufficient to develop psoriasis like inflammatory skin lesions [ 143 ].
16104843	vegf a	vegf a	1.0	moreover heterozygous vegf a transgenic mice which do not spontaneously develop inflammatory skin lesions are unable to down regulate experimentally induced inflammation and exhibit a psoriasis like phenotype characterized by ep
16104843	vegf a	vegf a	1.0	local production of vegf a in arthritic synovial tissue has been documented [ 16 ] and appears to correlate with disease activity in humans.
16104843	vegf a	vegf a	1.0	subsequently vegf a has been shown to be important in the pathogenesis of ra rheumatoid arthritis in animal models [ 146 148 ].
16104843	vegf a	vegf a	1.0	exaggerated levels of vegf a have been detected in tissues and biological samples from people with asthma where these levels correlate directly with disease [ 149 ] and inversely with airway function [ 150 ].
16104843	vegf a	vegf a	1.0	a recent study using lung targeted vegf 165 transgenic mice has revealed a novel function of vegf a in allergic responses.
16104843	vegf a	vegf a	1.0	in these mice vegf a induces asthma like inflammation airway and vascular remodelling and airway hyper responsiveness.
16104843	vegf a	vegf a	1.0	vegf a also enhances respiratory sensitization to antigen as well as t h 2 t helper type 2 cell mediated inflammation and increases the number of activated dendritic cells [ 151 ].
16104843	vegf a	vegf a	1.0	thus vegf a has a critical role in pulmonary t h 2 inflammation.
16104843	vegf a	vegf a	1.0	other studies have provided evidence for a role for vegf a as a pro inflammatory mediator in allograft rejection [ 152 ] and neointimal formation [ 153 ].
16104843	vegf a	vegf a	1.0	vegf a mrna expression not normally found in the adult mouse brain is up regulated after cerebral ischaemia and elevated vegf a levels can be detected as early as 3 h after stroke with a peak between 12 and 48 h [ 154 ].
16104843	vegf a	vegf a	1.0	previous studies have demonstrated that the antagonism of vegf a results in reduced oedema and tissue damage after ischaemia implicating vegf a in the pathophysiology of stroke [ 155 ].
16104843	vegf a	vegf a	1.0	paul et al. [ 156 ] have reported that src mice are resistant to vegf a induced vascular permeability and show decreased infarct volumes after stroke.
16104843	vegf a	vegf a	1.0	systemic application of a src inhibitor suppresses vascular permeability protecting wild type mice from ischaemia induced brain damage without influencing vegf a expression.
16104843	vegf a	vegf a	1.0	however sun et al. [ 157 ] have reported that intracerebroventricular administration of vegf a reduces infarct size improves neurological performance and enhances the delayed survival of newborn neurons.
16104843	vegf a	vegf a	1.0	these conflicting results appear to reflect dual roles of vegf a in stroke: neuroprotective and pro inflammatory effects.
16104843	vegf a	vegf a	1.0	in this context when infused through the internal carotid artery low and intermediate doses of vegf a significantly promote neuroprotection of the ischaemic brain whereas a high dose of vegf a offers no neuroprotection to the ischaemic brain or the damaged neurons of normal brain [ 158 ].
16104843	vegf a	vegf a	1.0	further studies are required for the therapeutic application of vegf a against stroke.
16104843	vegf a	vegf a	1.0	a subsequent study has revealed that vegf a is a modifier associated with motor neuron degeneration in human als and in a mouse model of als [ 162 ].
16104843	vegf a	vegf a	1.0	vegf a treatment increases the life expectancy of als mice without causing toxic side effects [ 163 164 ] indicating that vegf a has neuroprotective effects on motor neurons and treatment with vegf a could be one of the most effective therapies for als reported so far.
16104843	vegf a	vegf a	1.0	vegf a has no direct mitogenic effect on hepatocytes.
16104843	vascular endothelial growth factor	vascular endothelial growth factor	1.0	key words: angiogenesis inflammation signal transduction tumour vascular endothelial growth factor vegf vascular permeability.
16104843	vascular endothelial growth factor	vascular endothelial growth factor	1.0	wth factor; pvhl von hippel lindau tumour suppressor protein; ra rheumatoid arthritis; rtk receptor tyrosine kinase; s6k s6 kinase; tag t antigen; t h 2 t helper type 2; utr untranslated region; vegf vascular endothelial growth factor; vegfr vegf receptor; svegfr 1 soluble vegfr 1; svvegf snake venom vegf; tf svvegf trimeresurus flavoviridis svvegf; vpf vascular permeability factor.
16104843	vascular permeability factor	vascular permeability factor	1.0	elper type 2; utr untranslated region; vegf vascular endothelial growth factor; vegfr vegf receptor; svegfr 1 soluble vegfr 1; svvegf snake venom vegf; tf svvegf trimeresurus flavoviridis svvegf; vpf vascular permeability factor.
16104843	vascular endothelial growth factor	vascular endothelial growth factor	1.0	the vegf vascular endothelial growth factor family and its receptors are essential regulators of angiogenesis and vascular permeability.
16104843	vegf a	vegf a	1.0	currently the vegf family consists of vegf a plgf placenta growth factor vegf b vegf c vegf d vegf e and snake venom vegf.
16104843	vegf a	vegf a	1.0	vegf a has at least nine subtypes due to the alternative splicing of a single gene.
16104843	vegf a	vegf a	1.0	vegf a binds to and activates two tyrosine kinase receptors vegfr vegf receptor 1 and vegfr 2.
16104843	vegf a	vegf a	1.0	in solid tumours vegf a and its receptor are involved in carcinogenesis invasion and distant metastasis as well as tumour angiogenesis.
16104843	vegf a	vegf a	1.0	vegf a also has a neuroprotective effect on hypoxic motor neurons and is a modifier of als amyotrophic lateral sclerosis .
16104843	vascular endothelial growth factor a	vascular endothelial growth factor a	1.0	vascular endothelial growth factor a|receptors vascular endothelial growth factor|
16380619	vascular endothelial growth factor	vascular endothelial growth factor	1.0	hypoxia activates the endothelial cells to release inflammatory mediators and growth factors such as vascular endothelial growth factor vegf thought to play a role in the pathophysiology of sporadic als.
16533145	vascular endothelial growth factor	vascular endothelial growth factor	1.0	several other genes have been implicated as risk factors in motor neuron diseases including neurofilaments cytoplasmic dynein and dynactin vascular endothelial growth factor and angiogenin.
17015226	vascular endothelial growth factor	vascular endothelial growth factor	1.0	vascular endothelial growth factor vegf
17015226	vascular endothelial growth factor	vascular endothelial growth factor	1.0	vascular endothelial growth factor vegf an established regulator of developmental hypoxia induced and tumor induced angiogenesis gained interest as a contributor to als when deletion of the hypoxia response element hre in the murine v
17127558	vascular endothelial growth factor	vascular endothelial growth factor	1.0	d with transcription followed by those involved in antioxidant systems inflammation regulation of motor neuron function lipid metabolism protease inhibition and protection against apoptosis including vascular endothelial growth factor.
17582695	vascular endothelial growth factor	vascular endothelial growth factor	1.0	il 1beta and hypoxia inducible factor 1 hif 1 play important roles in influencing vessel plasticity along with vascular endothelial growth factor vegf [22] .