INT265803

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Context Info
Confidence 0.41
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 2.85
Pain Relevance 0.10

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
endothelial cells 4
plasma 2
FLT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
fibrosis 6 89.28 High High
cytokine 9 52.28 Quite High
bradykinin 11 22.64 Low Low
agonist 1 19.16 Low Low
dexamethasone 10 5.00 Very Low Very Low Very Low
antagonist 5 5.00 Very Low Very Low Very Low
Inflammation 4 5.00 Very Low Very Low Very Low
Central nervous system 3 5.00 Very Low Very Low Very Low
addiction 3 5.00 Very Low Very Low Very Low
metalloproteinase 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Adult Respiratory Distress Syndrome 28 98.32 Very High Very High Very High
Hypoxia 11 97.88 Very High Very High Very High
Nicotine Addiction 1 93.04 High High
Pre-eclampsia 33 91.16 High High
Pulmonary Fibrosis 1 90.96 High High
Fibromyalgia 4 87.28 High High
Cancer 53 82.04 Quite High
Lung Injury 4 77.12 Quite High
Peripheral Arterial Disease 18 74.88 Quite High
Solid Tumor 16 74.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 (source) of Positive_regulation (elevated) of sVEGFR1 in plasma associated with hypoxia
1) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.24 Pain Relevance 0
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 (necessary) of Positive_regulation (activation) of VEGFR-2 in endothelial cells
2) Confidence 0.31 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.73 Pain Relevance 0.03
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 (sufficient) of Positive_regulation (activation) of VEGFR-2 in endothelial cells
3) Confidence 0.31 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.73 Pain Relevance 0.03
However, binding of VEGF to cell transmembrane receptors is reduced by a soluble circulating form of Flt-1 (sFlt-1), which is generated by alternative splicing.
Positive_regulation (generated) of Positive_regulation (circulating) of sFlt-1
4) Confidence 0.19 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2739214 Disease Relevance 0.43 Pain Relevance 0
Increased levels of soluble VEGFR-1(s-flt) have been demonstrated to contribute to these observations (23).
Positive_regulation (contribute) of Positive_regulation (Increased) of VEGFR-1
5) Confidence 0.10 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.72 Pain Relevance 0.04

General Comments

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