INT199567

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Context Info
Confidence 0.47
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 18
Total Number 19
Disease Relevance 13.81
Pain Relevance 1.34

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

plasma membrane (Kdr) kinase activity (Kdr) cytoplasm (Kdr)
Anatomy Link Frequency
vasculature 3
endothelial cells 1
edge 1
synovium 1
Atlas 1
Kdr (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 108 99.32 Very High Very High Very High
rheumatoid arthritis 116 98.80 Very High Very High Very High
antagonist 17 94.68 High High
cytokine 97 93.40 High High
imagery 102 91.28 High High
Osteoarthritis 6 88.20 High High
ischemia 35 74.48 Quite High
Kinase C 6 72.12 Quite High
anesthesia 10 61.84 Quite High
Inflammatory response 5 61.00 Quite High
Disease Link Frequency Relevance Heat
Fibromyalgia 3 100.00 Very High Very High Very High
Renal Cell Carcinoma 50 99.84 Very High Very High Very High
INFLAMMATION 112 99.32 Very High Very High Very High
Cancer 729 99.28 Very High Very High Very High
Pancreatic Cancer 41 99.04 Very High Very High Very High
Metastasis 125 98.96 Very High Very High Very High
Rheumatoid Arthritis 121 98.80 Very High Very High Very High
Acute Liver Failure 44 98.56 Very High Very High Very High
Malignant Neoplastic Disease 11 98.36 Very High Very High Very High
Hemangiosarcoma 6 97.92 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
FLT1 (VEGFR1) and KDR/FLK1 (VEGFR2) are the major receptors which bind VEGFA.
KDR Binding (bind) of
1) Confidence 0.47 Published 2010 Journal Cancer management and research Section Body Doc Link PMC3004565 Disease Relevance 0.67 Pain Relevance 0
Specifically, VEGF145, the major tumor-associated isoform, will inhibit the binding of VEGF165 to the KDR/FLK1 receptor.24 Additionally, VEGF regulates the permeability of blood vessels,25 in a dose dependent manner.
KDR Binding (binding) of in blood vessels associated with cancer
2) Confidence 0.35 Published 2010 Journal Cancer management and research Section Body Doc Link PMC3004565 Disease Relevance 0.66 Pain Relevance 0
On a related note, sVEGFR-3 can not only bind VEGFR-3 but also acts as a trap for VEGF-C, which blocks VEGFR-3 signaling [2,5].
sVEGFR-3 Binding (bind) of
3) Confidence 0.27 Published 2010 Journal BMC Med Section Body Doc Link PMC2989928 Disease Relevance 1.12 Pain Relevance 0.05
Oligonucleotides coding shRNA for mouse Rac1, mouse VEGFR2/Flk-1, ?
Flk-1 Binding (coding) of
4) Confidence 0.27 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842301 Disease Relevance 0 Pain Relevance 0
We have shown that IQGAP1 translocates to the leading edge where it binds to VEGFR2 and NADPH oxidase2, a major source of ROS in ECs, thereby promoting ROS production and directional EC migration [18], [20].
VEGFR2 Binding (binds) of in edge
5) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.45 Pain Relevance 0.12
First, VEGF165 binding to KDR may lead to an increase in angiogenesis, and thereby, the recruitment of peripheral leukocytes to inflamed synovium, which diminishes the growing burden of synoviocytes by supplying the oxygen and nutrients required for tissue metabolism.
KDR Binding (binding) of in synovium
6) Confidence 0.25 Published 2008 Journal Mediators of Inflammation Section Body Doc Link PMC2638142 Disease Relevance 1.12 Pain Relevance 0.50
VEGF165 exerts its biological effects by binding with its receptor subtypes, that is, fms-like tyrosine kinase (Flt-1), kinase insert domain-containing receptor (KDR) and neuropilin-1 (NP-1) [3].
KDR Binding (binding) of associated with fibromyalgia
7) Confidence 0.24 Published 2008 Journal Mediators of Inflammation Section Body Doc Link PMC2638142 Disease Relevance 1.14 Pain Relevance 0.34
The Nrps can also bind to certain heparin binding isofoms of VEGF (e.g., VEGF165) to enhance the binding of VEGF to VEGFR1, and VEGFR2 (Figure 1) [31, 32].
VEGFR2 Binding (binding) of
8) Confidence 0.20 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2902148 Disease Relevance 0.67 Pain Relevance 0.08
A second mechanism of TK dysfunction in malignant cells is via the overexpression of a TK or its ligand; eg, the overexpression of VEGFR, PDGFR, or EGFR or their ligands in RCC (Gomella et al 1989; Mydlo et al 1989; Atlas et al 1992; Uhlman et al 1995; Iliopoulos et al 1996; Ramp et al 2000; Gunningham et al 2001; Na et al 2003; Sulzbacher et al 2003, Yildiz et al 2004; Minardi et al 2005; Xu et al 2005).
VEGFR Binding (ligands) of in Atlas associated with malignant neoplastic disease and renal cell carcinoma
9) Confidence 0.17 Published 2006 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC1661649 Disease Relevance 0.67 Pain Relevance 0.04
We found that targeting to VEGFR2, endoglin, or the VEGF:VEGFR complex was specific for tumor vasculature as there was no signal enhancement in nontumor tumor tissue.
VEGFR Binding (complex) of in vasculature associated with cancer
10) Confidence 0.15 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2902148 Disease Relevance 1.16 Pain Relevance 0.04
We found that targeting to VEGFR2, endoglin, or the VEGF:VEGFR complex was specific for tumor vasculature as there was no signal enhancement in nontumor tumor tissue.
VEGFR2 Binding (targeting) of in vasculature associated with cancer
11) Confidence 0.15 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2902148 Disease Relevance 1.17 Pain Relevance 0.04
VEGFR2 is a commonly used marker of vascular endothelial cells and has been used by multiple groups as a molecular target for MB.
VEGFR2 Binding (target) of in endothelial cells
12) Confidence 0.15 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2902148 Disease Relevance 1.44 Pain Relevance 0.08
The cells were then trypsinized for 1 minute, centrifuged, washed with PBS, fixed in 4% paraformaldehyde for 0.5 hour at room temperature, washed and blocked in 2%FCS for 0.5 hour at room temperature with agitation. 1.5×105cells were then incubated with each of the following conjugated monoclonal antibodies: Tie-2, Flk-1, CD34, c-Kit, Thy-1, Sca-1 (PharMingen, San Diego, CA) for 90 mins at room temperature.
Flk-1 Binding (temperature) of
13) Confidence 0.10 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762397 Disease Relevance 0.30 Pain Relevance 0.06
These co-ordinate effects by VEGF and VEGFR interaction should contribute to decrease the overall survival of the R2-mAb-treated group with AHF in the current study.
VEGFR Binding (interaction) of associated with acute liver failure
14) Confidence 0.07 Published 2010 Journal J Angiogenes Res Section Body Doc Link PMC2933582 Disease Relevance 0.50 Pain Relevance 0
These results indicated that VEGF-VEGFR interaction was a major regulator in the maintenance of the SEC architecture in Gal-N+LPS-induced AHF.
VEGFR Binding (interaction) of associated with acute liver failure
15) Confidence 0.07 Published 2010 Journal J Angiogenes Res Section Body Doc Link PMC2933582 Disease Relevance 0.48 Pain Relevance 0
Characterization of the cells for their immunophenotypic markers by fluorescent-activated cell sorting (FACS) showed that they were negative for cell lineage markers CD45, CD14, CD34, CD19, CD3, Flk-1 and positive for typical MSC surface proteins Sca-1, CD105, CD29, CD90, CD73 and CD44 (Table 1).
Flk-1 Binding (negative) of
16) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2270908 Disease Relevance 0.30 Pain Relevance 0
Characterization of the cells for their immunophenotypic markers by fluorescent-activated cell sorting (FACS) showed that they were negative for cell lineage markers CD45, CD14, CD34, CD19, CD3, Flk-1 and positive for typical MSC surface proteins Sca-1, CD105, CD29, CD90, CD73 and CD44 (Table 1).
Flk-1 Neg (negative) Binding (lineage) of
17) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2270908 Disease Relevance 0.30 Pain Relevance 0
Both agents are derived from the same mouse monoclonal antibody precursor and show high affinity for VEGF, neutralizing its effects by binding to VEGF and preventing VEGFR interaction.
VEGFR Binding (interaction) of
18) Confidence 0.04 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350125 Disease Relevance 0.62 Pain Relevance 0
Fukusawa et al previously reported that pancreatic tumor growth and metastasis in vivo were significantly suppressed by a soluble VEGFR chimer which binds VEGF-A with high affinity [35].
VEGFR Binding (binds) of associated with pancreatic cancer and metastasis
19) Confidence 0.02 Published 2010 Journal J Exp Clin Cancer Res Section Body Doc Link PMC2893453 Disease Relevance 1.05 Pain Relevance 0

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