INT143442

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Context Info
Confidence 0.57
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 15
Disease Relevance 2.62
Pain Relevance 0.30

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 2
SK-MEL-28 1
NRP1 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 18 99.60 Very High Very High Very High
Inflammation 52 75.52 Quite High
Inflammatory marker 2 75.00 Quite High
rheumatoid arthritis 54 50.00 Quite Low
Snapping jaw 2 50.00 Quite Low
metalloproteinase 21 7.84 Low Low
addiction 18 5.00 Very Low Very Low Very Low
cytokine 12 5.00 Very Low Very Low Very Low
ischemia 12 5.00 Very Low Very Low Very Low
Infliximab 8 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Leukemia 12 100.00 Very High Very High Very High
Neurodegenerative Disease 1 100.00 Very High Very High Very High
Melanoma 73 93.94 High High
Frailty 2 85.80 High High
Hypercalcemia 34 79.76 Quite High
Hypoxia 23 76.32 Quite High
INFLAMMATION 56 75.52 Quite High
Vasculitis 6 75.12 Quite High
Endometriosis (extended) 22 73.16 Quite High
Eclampsia 18 72.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Possible candidates include: (a) human soluble VEGFR2 (160 kDa) – present in significant quantities in healthy human plasma (7–8 ng/mL) [140] and upregulated in acute myeloid leukemia [39]; (b) soluble NRP1 (90 kDa) – a VEGF165-specific antagonist, with documented renal expression in humans [141], [142]; and (c) cellular fibronectin (?
Positive_regulation (upregulated) of NRP1 in plasma associated with leukemia and antagonist
1) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.24 Pain Relevance 0.05
However, the presence of VEGF165b did significantly reduce the VEGF165-stimulated increase in cell number (10 ng/ml VEGF165 and VEGF165b, P < 0.01, 20 ng/ml VEGF165 and VEGF165b, P < 0.01; Fig. 5B).
Positive_regulation (increase) of VEGF165b
2) Confidence 0.43 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.18 Pain Relevance 0
However, the presence of VEGF165b did significantly reduce the VEGF165-stimulated increase in cell number (10 ng/ml VEGF165 and VEGF165b, P < 0.01, 20 ng/ml VEGF165 and VEGF165b, P < 0.01; Fig. 5B).
Positive_regulation (increase) of VEGF165
3) Confidence 0.43 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.12 Pain Relevance 0
However, the presence of VEGF165b did significantly reduce the VEGF165-stimulated increase in cell number (10 ng/ml VEGF165 and VEGF165b, P < 0.01, 20 ng/ml VEGF165 and VEGF165b, P < 0.01; Fig. 5B).
Positive_regulation (increase) of VEGF165b
4) Confidence 0.43 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.19 Pain Relevance 0
However, the presence of VEGF165b did significantly reduce the VEGF165-stimulated increase in cell number (10 ng/ml VEGF165 and VEGF165b, P < 0.01, 20 ng/ml VEGF165 and VEGF165b, P < 0.01; Fig. 5B).
Positive_regulation (increase) of VEGF165
5) Confidence 0.43 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.19 Pain Relevance 0
However, the presence of VEGF165b did significantly reduce the VEGF165-stimulated increase in cell number (10 ng/ml VEGF165 and VEGF165b, P < 0.01, 20 ng/ml VEGF165 and VEGF165b, P < 0.01; Fig. 5B).
Positive_regulation (increase) of VEGF165
6) Confidence 0.43 Published 2010 Journal American Journal of Physiology - Lung Cellular and Molecular Physiology Section Body Doc Link PMC2886605 Disease Relevance 0.18 Pain Relevance 0
This in turn increased availability of free VEGF165 for direct VEGFR1-binding (Fig. 6D).
Positive_regulation (increased) of VEGF165
7) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Moreover, increasing NRP1 density shifted the VEGF-signaling profiles as shown in Fig. 5B.
Positive_regulation (increasing) of NRP1
8) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Possible candidates include: (a) human soluble VEGFR2 (160 kDa) – present in significant quantities in healthy human plasma (7–8 ng/mL) [140] and upregulated in acute myeloid leukemia [39]; (b) soluble NRP1 (90 kDa) – a VEGF165-specific antagonist, with documented renal expression in humans [141], [142]; and (c) cellular fibronectin (?
Positive_regulation (upregulated) of VEGF165 in plasma associated with leukemia and antagonist
9) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.25 Pain Relevance 0.05
On the other hand, the overall rise in “pro-angiogenic potential”, as represented by ligated VEGFR2 complexes, can be explained by NRP1's role as a co-receptor in presenting NRP1-bound VEGF165 to VEGFR2, as well as in stabilizing VEGF165-VEGFR2 through their triplet configuration.
Positive_regulation (stabilizing) of VEGF165
10) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Overall, increasing NRP1 density, increasing VEGFR2?
Positive_regulation (increasing) of NRP1
11) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Hierarchical clustering using only the 106 transcripts identified by class comparison revealed two main expression motifs in the melanoma cell lines (Figure 1A): Motif 1 distinguished eight cell lines (NZM09, NZM11, NZM19, NZM22, NZM40, NZM52, SK-MEL-28, UACC62), and consisted of down-regulation of genes involved in neural crest and melanocyte development, differentiation, and pigmentation (e.g., EDNRB, MITF, MLANA, TYR; Table S1), and up-regulation of genes related to angiogenesis, neurogenesis, immunomodulation, and interaction and remodelling of the extracellular environment (e.g., HIF1a, NRP1, PLAUR, TGFBI; Table S1); Motif 2 distinguished the remaining 19 cell lines, and showed a pattern of gene expression that tended to be the inverse of Motif 1, with down-regulation of extracellular remodelling genes and up-regulation of MITF and melanocyte lineage markers, although not all Motif 2 cell lines had higher levels of MITF expression (e.g.
Positive_regulation (up-regulation) of NRP1 in SK-MEL-28 associated with melanoma and neurodegenerative disease
12) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794539 Disease Relevance 0.33 Pain Relevance 0
In response to hypoxia, VEGF121 and VEGF165 mRNA were both remarkably increased, while there was no change in VEGF mRNA stability.
Positive_regulation (increased) of VEGF165
13) Confidence 0.04 Published 2007 Journal J. Oral Pathol. Med. Section Body Doc Link 17448139 Disease Relevance 0.15 Pain Relevance 0
However, 11% of the women had elevated P1NP (reference values for men not available), 8% of the patients had elevated CTX-1 and 38% had elevated 1CTP.
Positive_regulation (elevated) of P1NP
14) Confidence 0.01 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2656227 Disease Relevance 0.29 Pain Relevance 0
In the NoP-group reduction of CRP from 0 to 3 months correlated with increase in P1NP from 0 to 3 months (r = -0.39, p = 0.001), as well as with increase in 1CTP (r = -0.36, p = 0.003).
Positive_regulation (increase) of P1NP
15) Confidence 0.01 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2656227 Disease Relevance 0.48 Pain Relevance 0.20

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