INT143127

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Context Info
Confidence 0.66
First Reported 2007
Last Reported 2010
Negated 0
Speculated 3
Reported most in Body
Documents 44
Total Number 48
Disease Relevance 21.70
Pain Relevance 1.92

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

cell differentiation (FLT1) endosome (FLT1) Golgi apparatus (FLT1)
cytoplasm (FLT1) extracellular space (FLT1) extracellular region (FLT1)
Anatomy Link Frequency
plasma 6
blood 4
placenta 2
endothelial cells 1
colon 1
FLT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
positron emission tomography 53 97.72 Very High Very High Very High
Pain 19 96.76 Very High Very High Very High
cINOD 1 93.84 High High
antagonist 71 93.56 High High
Restless leg syndrome 20 90.72 High High
ischemia 104 90.00 High High
cva 200 88.80 High High
metalloproteinase 65 87.92 High High
addiction 61 87.60 High High
fibrosis 11 85.76 High High
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 147 100.00 Very High Very High Very High
Fibromyalgia 42 100.00 Very High Very High Very High
Pre-eclampsia 980 99.84 Very High Very High Very High
Colon Cancer 2 99.84 Very High Very High Very High
Cancer 550 99.12 Very High Very High Very High
Stress 72 99.00 Very High Very High Very High
Sickle Cell Anemia 6 98.84 Very High Very High Very High
Adult Respiratory Distress Syndrome 36 98.32 Very High Very High Very High
Peripheral Arterial Disease 364 98.28 Very High Very High Very High
Systemic Lupus Erythematosus 9 97.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The former effects increased quantities of non-NRP1-coupled VEGF-VEGFR complexes with increasing total VEGFR density, despite the diminishing fractional occupancies of VEGFRs (Fig. 5D).
Positive_regulation (ts increa) of VEGFR density
1) Confidence 0.66 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0.04
Increases in soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sEng) contribute to the pathogenesis of pre-eclampsia.
Positive_regulation (Increases) of sFlt-1 associated with fibromyalgia and eclampsia
2) Confidence 0.59 Published 2009 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 19215236 Disease Relevance 0.35 Pain Relevance 0.06
Increases in soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sEng) contribute to the pathogenesis of pre-eclampsia.
Positive_regulation (Increases) of soluble fms-like tyrosine kinase 1 associated with fibromyalgia and eclampsia
3) Confidence 0.59 Published 2009 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 19215236 Disease Relevance 0.35 Pain Relevance 0.06
This may suggest that hypoxia-induced secretion of sVEGFR1 (as opposed to lymphatic drainage of sVEFR1) is indeed the faster and major source of elevated plasma sVEGFR1 in exercise; but our simulations were unable to confirm the conclusion by Bailey et al. [49] that VEGF trapping by the surge of sVEGFR1 had caused the drop in plasma VEGF.
Positive_regulation (elevated) of sVEGFR1 in plasma associated with hypoxia
4) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.24 Pain Relevance 0
Secondly, the transendothelial gradient of sVEGFR1 at control favored net extravasation, hence increasing kP resulted in: lower plasma concentrations of free sVEGFR1; as well as increased free sVEGFR1 in the interstitium facing the endothelium where kP was upregulated, at the expense of a decrease in interstitial free sVEGFR1 in the other tissue compartment (e.g., “Control” vs.
Positive_regulation (increased) of sVEGFR1 in endothelium
5) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
This was due to a secondary “spill-over” of the elevated plasma free sVEGFR1 through increased extravasation into the distal compartment.
Positive_regulation (elevated) of sVEGFR1 in plasma
6) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.15 Pain Relevance 0
Distribution changes were again more evident in the blood: the simultaneous elevations in free VEGF and sVEGFR1, due to increasing global kL (e.g., 10× from control), in turn synergistically increased sVEGFR1-VEGF complex formation (e.g., 88× from control), which elevated the complexed fractions of both VEGF (e.g., +13%) and sVEGFR1 (e.g., +8.7%).
Positive_regulation (elevations) of sVEGFR1 in blood
7) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.15 Pain Relevance 0
This may suggest that if increasing kL were to be explored as a therapeutic means to alleviate calf tissue accumulation of sVEGFR1, local lymphatic flushing as induced by leg exercise may be more productive than whole-body exercise (Fig. 9A).
Positive_regulation (accumulation) of sVEGFR1 in body associated with increased venous pressure under development
8) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.16 Pain Relevance 0
Lowering NRP1's affinity for VEGF165 over two orders of magnitude – Kd(V165,N) from 200 pM to 25 nM –caused only opposing changes of up to 0.3% in the VEGF-bound fractional occupancies of VEGFR1 and VEGFR2 (Fig. 6D).
Positive_regulation (occupancies) of VEGFR1
9) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
This in turn increased availability of free VEGF165 for direct VEGFR1-binding (Fig. 6D).
Positive_regulation (increased) of VEGFR1-binding
10) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The latter effects stemmed from an increasing proportion of total NRP1 being used up in formation of unligated VEGFR1-NRP1 complexes with increasing total VEGFR density (Fig. 5E).
Positive_regulation (increasing) of VEGFR density
11) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0.04
VEGFR-1 (ligands include VEGF-A, -B, and placental growth factor [PIGF]) and VEGFR-2 (ligands include VEGF-A, -C, and -D) are predominantly expressed on vascular endothelial cells, and activation of VEGFR-2 appears to be both necessary and sufficient to mediate VEGF-dependent angiogenesis and induction of vascular permeability [13, 14].
Positive_regulation (activation) of VEGFR-2 in endothelial cells
12) Confidence 0.46 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.73 Pain Relevance 0.03
Most of the Flt-1 produced in the mouse and human placenta during later stages of gestation is the soluble form (sFlt-1) generated by alternative splicing of Flt-1, leading to a premature termination after the sixth Ig-like domain [30]. sFlt-1 binds both VEGF and PlGF and acts as a soluble antagonist of their action.
Positive_regulation (generated) of sFlt-1 in placenta associated with antagonist
13) Confidence 0.46 Published 2008 Journal BMC Med Genet Section Body Doc Link PMC2496902 Disease Relevance 0.55 Pain Relevance 0.05
Intramuscular production of sVEGFR1 was assumed in this model to occur entirely through abluminal endothelial secretion into the interstitium; luminal endothelial secretion into the circulation is a conceivable direct blood source of sVEGFR1 but has yet to be quantitatively documented.
Positive_regulation (source) of sVEGFR1 in blood
14) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.35 Pain Relevance 0.15
Hence, consecutive “active days” negligibly enhanced the peak sVEGFR1 level attainable in subsequent “active days” (+44 pM sVEGFR1; +1.0 pM VEGF relative to control).

6.4.

Positive_regulation (enhanced) of sVEGFR1
15) Confidence 0.41 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.
Positive_regulation (elevated) of sVEGFR1
16) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Hence we hypothesized that the physiological activity-dependent fluctuations in lymphatic drainage rates may contribute to the clinical heterogeneity observed in plasma measurements of VEGF and sVEGFR1.
Positive_regulation (measurements) of sVEGFR1 in plasma
17) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.41 Pain Relevance 0.09
Changing levels of circulating sVEGFR1 may reflect altered tissue expression of surface receptors
Positive_regulation (circulating) of sVEGFR1
18) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Since lymph flow represented a unidirectional flushing of VEGF and sVEGFR1 from the interstitium into blood, increasing kL resulted in higher plasma and lower interstitial concentrations of free VEGF and sVEGFR1.
Positive_regulation (flushing) of sVEGFR1 in plasma associated with increased venous pressure under development
19) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.10 Pain Relevance 0
Hence, consecutive “active days” negligibly enhanced the peak sVEGFR1 level attainable in subsequent “active days” (+44 pM sVEGFR1; +1.0 pM VEGF relative to control).

6.4.

Positive_regulation (enhanced) of sVEGFR1
20) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0

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