INT191718

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Context Info
Confidence 0.50
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 35
Total Number 35
Disease Relevance 12.18
Pain Relevance 0.27

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytoplasm (FLT1, VEGFA) extracellular space (FLT1, VEGFA) extracellular region (FLT1, VEGFA)
cell differentiation (FLT1) endosome (FLT1) Golgi apparatus (FLT1)
Anatomy Link Frequency
endothelial cells 2
muscle tissue 2
body 2
liver 1
vascular endothelium 1
FLT1 (Homo sapiens)
VEGFA (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 59 98.72 Very High Very High Very High
Bioavailability 1 78.64 Quite High
cytokine 44 72.36 Quite High
Pain 18 60.12 Quite High
aspirin 5 58.28 Quite High
Inflammation 23 49.56 Quite Low
bradykinin 22 45.20 Quite Low
ischemia 39 44.72 Quite Low
Restless leg syndrome 18 27.04 Quite Low
agonist 2 22.04 Low Low
Disease Link Frequency Relevance Heat
Cancer 531 100.00 Very High Very High Very High
Fibromyalgia 30 99.92 Very High Very High Very High
Apoptosis 18 98.80 Very High Very High Very High
Pre-eclampsia 305 96.92 Very High Very High Very High
Colon Cancer 37 96.72 Very High Very High Very High
Solid Tumor 52 94.40 High High
Disease 264 93.04 High High
Metastasis 39 92.88 High High
Pancreatic Cancer 150 89.72 High High
Pulmonary Disease 3 87.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
VEGF affinity of VEGFR1 and VEGFR2 varied from Kd?
VEGFR1 Binding (affinity) of VEGF
1) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Flow analysis (Fig. 4) suggested that the elevated interstitial free sVEGFR1 would then associate with free VEGF to form sVEGFR1-VEGF complexes, which accounted for the slight decreases in [V]IS in the direction of increasing local qsR1.
sVEGFR1 Binding (associate) of VEGF
2) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
In other words, while VEGF was mostly bound to sVEGFR1 in blood, almost all extracellular VEGF in muscle tissue was surface receptor- or matrix-bound.
sVEGFR1 Binding (bound) of VEGF in muscle tissue
3) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Higher NRP1 densities were generally associated with lower concentrations of all soluble species, since NRP1 was a vehicle for internalizing VEGF and sVEGFR1 via endothelial VEGF121-NRP1, VEGF165-NRP1, sVEGFR1-NRP1, VEGF121-VEGFR1-NRP1 complexes.
VEGFR1-NRP1 Binding (complexes) of VEGF
4) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
As for the soluble species, total free VEGF in all compartments decreased with increasing VEGF-binding affinity of either VEGFR1 or VEGFR2 – presumably through enhanced internalization of complexed VEGF (Fig. 6B).
VEGFR1 Binding (affinity) of VEGF-binding
5) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Higher NRP1 densities were generally associated with lower concentrations of all soluble species, since NRP1 was a vehicle for internalizing VEGF and sVEGFR1 via endothelial VEGF121-NRP1, VEGF165-NRP1, sVEGFR1-NRP1, VEGF121-VEGFR1-NRP1 complexes.
VEGFR1-NRP1 Binding (complexes) of VEGF121
6) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Given the in vitro evidence that the soluble and full-length VEGFR1's have similar affinities to VEGF [95], we assumed in our model a Kd of 33 pM for VEGF-sVEGFR1 binding, same as that previously used [54] for VEGF-VEGFR1 binding.
VEGFR1 Binding (affinities) of VEGF
7) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Flow analysis (Fig. 4) suggested that the elevated interstitial free sVEGFR1 would then associate with free VEGF to form sVEGFR1-VEGF complexes, which accounted for the slight decreases in [V]IS in the direction of increasing local qsR1.
sVEGFR1 Binding (associate) of sVEGFR1-VEGF
8) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
In this region, the greater abundance of VEGFR1 gave more prominence to NRP1's tendency to competitively shift the distribution of total VEGFR1 towards formation of unligated VEGFR1-NRP1 complexes, in the process freeing VEGF that had been bound to uncoupled VEGFR1, hence elevating free VEGF concentrations.
VEGFR1 Binding (bound) of VEGF
9) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
As for the soluble species, total free VEGF in all compartments decreased with increasing VEGF-binding affinity of either VEGFR1 or VEGFR2 – presumably through enhanced internalization of complexed VEGF (Fig. 6B).
VEGFR1 Binding (affinity) of VEGF
10) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Regarding the new sVEGFR1 interactions with VEGF, matrix sites and NRP1, the following assumptions were made for their kinetic rates.
sVEGFR1 Binding (interactions) of VEGF
11) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
In the blood, both VEGF121 and VEGF165 were 23% free and 77% bound to sVEGFR1 (Fig.
sVEGFR1 Binding (bound) of VEGF121 in blood
12) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
In other words, while VEGF was mostly bound to sVEGFR1 in blood, almost all extracellular VEGF in muscle tissue was surface receptor- or matrix-bound.
sVEGFR1 Binding (bound) of VEGF in muscle tissue
13) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Hence in seeking our control sVEGFR1-secretion rates, we redefined the control VEGF-secretion rates to qV,+Ctrl?
sVEGFR1 Binding (seeking) of VEGF-secretion
14) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
This implication that VEGF-trapping alone may not account for sVEGFR1's anti-angiogenic potential needs to be experimentally validated; while computationally, the next step would be to investigate whether heterodimerization with surface VEGFRs is the key to sVEGFR1's purported contribution in impaired angiogenesis.
sVEGFR1 Neg (not) Binding (account) of VEGF-trapping
15) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
To the extent that the present study focuses on sVEGFR1's effect on the formation of surface VEGF signaling complexes, the uncertainties in the characterization of matrix sites are not of concern.
sVEGFR1 Binding (formation) of VEGF
16) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
To model the systemic distributions of VEGF and sVEGFR1 associated with healthy subjects, a physiologically-based pharmacokinetic model was constructed that divided the human body into three compartments: (1) the “calf”, consisting of the gastrocnemius and soleus muscles; (2) the “normal (rest of the body)”, consisting of all other solid tissues; and (3) the “blood”, that interacts with the other two compartments.
sVEGFR1 Binding (associated) of VEGF in body
17) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.13 Pain Relevance 0
Hence we identified the need for a computational model that predicts the systemic distributions and molecular interactions of VEGF and sVEGFR1 across the human body, to serve as a platform for the mechanistic study of sVEGFR1's purported anti-angiogenic properties, as well as the pre-clinical study of sVEGFR1 as a disease marker and therapeutic agent.


sVEGFR1 Binding (interactions) of VEGF in body associated with disease
18) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.60 Pain Relevance 0
Although the exact contribution of VEGFR-1 signaling to angiogenesis is unclear, it has been shown that VEGFR-1 directly cooperates with VEGFR-2 via heterodimerization, as well as binding two additional VEGF homologues, VEGF-B and PIGF [19].
VEGFR-2 Binding (binding) of VEGF
19) Confidence 0.28 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.43 Pain Relevance 0
Although the exact contribution of VEGFR-1 signaling to angiogenesis is unclear, it has been shown that VEGFR-1 directly cooperates with VEGFR-2 via heterodimerization, as well as binding two additional VEGF homologues, VEGF-B and PIGF [19].
VEGFR-2 Binding (binding) of VEGF
20) Confidence 0.28 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.43 Pain Relevance 0

General Comments

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