INT265800

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Context Info
Confidence 0.75
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 14
Total Number 14
Disease Relevance 3.66
Pain Relevance 0.69

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 (NRP1) cytosol (NRP1) signal transduction (NRP1)
extracellular region (NRP1) cell adhesion (NRP1) plasma membrane (NRP1)
Anatomy Link Frequency
plasma 4
endothelial cell 2
reservoir 2
myocytes 1
cleavage 1
NRP1 (Homo sapiens)
Pain Link Frequency Relevance Heat
metalloproteinase 34 99.54 Very High Very High Very High
Bioavailability 1 86.12 High High
ischemia 22 77.60 Quite High
Inflammation 54 69.04 Quite High
cytokine 14 55.36 Quite High
antagonist 34 52.92 Quite High
Inflammatory mediators 2 51.76 Quite High
tolerance 11 14.60 Low Low
addiction 33 5.00 Very Low Very Low Very Low
Central nervous system 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 140 99.08 Very High Very High Very High
Peripheral Arterial Disease 198 98.72 Very High Very High Very High
Hemangiosarcoma 139 97.56 Very High Very High Very High
Chronic Sinusitis 55 90.08 High High
Coronary Artery Disease 66 87.12 High High
Syndrome 5 85.20 High High
Hematoma 22 81.20 Quite High
Food Poisoning 1 80.28 Quite High
Fibromyalgia 11 80.24 Quite High
Injury 12 77.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
VEGF165 (lacking exon 6 but not 7) has some heparin-binding affinity and so upon secretion exists in equilibrium between soluble and cell-associated forms.
Localization (secretion) of VEGF165
1) Confidence 0.75 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.11 Pain Relevance 0.04
0), the steady-state plasma and interstitial free VEGF concentrations ([V]pl, [V]IS) were mapped out as functions of total VEGF-secretion rates from the normal tissue and calf compartments (qTotalVEGF,Normal and qTotalVEGF,Calf), where the individual isoforms VEGF121 and VEGF165 were secreted at a ratio of 1?
Localization (secreted) of VEGF165 in plasma
2) Confidence 0.66 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Release of VEGF165 from interstitial matrix sites through plasmin/MMP degradation of matrix core proteins was also neglected.
Localization (Release) of VEGF165 associated with metalloproteinase
3) Confidence 0.66 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.28 Pain Relevance 0.14
Simultaneously in all fluid volumes, free VEGF121 levels remained consistent while free VEGF165, presumably released from NRP1s, elevated slightly (plasma data shown in Fig. 6E).
Localization (released) of VEGF165 in plasma
4) Confidence 0.66 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Densities and VEGF-affinity of interstitial matrix sites affected only matrix-bound reservoirs of VEGF165 and sVEGFR1
Localization (reservoirs) of VEGF165 in reservoirs
5) Confidence 0.66 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Among the major endothelial cell surface receptor targets for these VEGF isoforms are: the tyrosine kinases VEGFR1 (Flt-1; UniProt accession P17948-1) and VEGFR2 (mouse Flk-1; human KDR; UniProt accession P35968); as well as the co-receptor neuropilin-1 (NRP1; UniProt accession O14786), which couples directly with VEGFR1, and indirectly with VEGFR2 through non-overlapping binding sites on VEGF165 [7].


Localization (targets) of neuropilin-1 in endothelial cell
6) Confidence 0.62 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.48 Pain Relevance 0.03
Among the major endothelial cell surface receptor targets for these VEGF isoforms are: the tyrosine kinases VEGFR1 (Flt-1; UniProt accession P17948-1) and VEGFR2 (mouse Flk-1; human KDR; UniProt accession P35968); as well as the co-receptor neuropilin-1 (NRP1; UniProt accession O14786), which couples directly with VEGFR1, and indirectly with VEGFR2 through non-overlapping binding sites on VEGF165 [7].


Localization (targets) of NRP1 in endothelial cell
7) Confidence 0.62 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.48 Pain Relevance 0.03
Moreover, interstitial proteolytic clearance of soluble or matrix-bound VEGF – e.g., plasmin- and matrix metalloproteinase (MMP)-mediated cleavage of VEGF165 and the respective release of VEGF110 and VEGF113 fragments [95], [146], as well as the intrinsic protein degradation rate of VEGF [147] – was not considered in the current model.
Localization (release) of VEGF165 in cleavage associated with metalloproteinase
8) Confidence 0.62 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.33 Pain Relevance 0.17
Abnormal plasma levels of MMPs in PAD [148], [149] may suggest a role for proteolytic degradation or release of VEGF165 in causing pathological bioavailabilities of VEGF.
Localization (release) of VEGF165 in plasma associated with peripheral arterial disease
9) Confidence 0.58 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.16 Pain Relevance 0.13
Within the tissue compartments, free VEGF121 and VEGF165 were secreted from parenchymal cells (myocytes) in a 1?
Localization (secreted) of VEGF165 in myocytes
10) Confidence 0.58 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.15 Pain Relevance 0.04
In contrast, the quantities of matrix-bound VEGF165 and sVEGFR1 increased drastically with increasing matrix site densities (Fig. 7A,B); while the matrix-bound reservoir of VEGF165 also grew drastically with higher VEGF165-affinity of matrix sites (Fig. 7A).
Localization (reservoir) of VEGF165 in reservoir
11) Confidence 0.58 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Simultaneously in all fluid volumes, free VEGF121 levels remained consistent while free VEGF165, presumably released from NRP1s, elevated slightly (plasma data shown in Fig. 6E).
Localization (released) of NRP1s in plasma
12) Confidence 0.58 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
It should be noted that out of the 9 CRSwNP patients where no se could be detected, 1, 4 and 4 were observed in NP1, NP2 and NP3, respectively.
Localization (observed) of NP1
13) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2832699 Disease Relevance 0.76 Pain Relevance 0.08
, CD44, and EPHA2 in hemangiosarcoma cell lines was not predictive for the expression of these proteins in tumor tissues (Figure 5B), and a similar trend was observed for Neuropilin 1 and v-Myc.
Localization (observed) of Neuropilin 1 associated with cancer and hemangiosarcoma
14) Confidence 0.04 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2994824 Disease Relevance 0.92 Pain Relevance 0.03

General Comments

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