INT337162

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Context Info
Confidence 0.32
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.98
Pain Relevance 0.28

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, Iqgap1) cytoplasm (Kdr, Iqgap1) nucleus (Iqgap1)
protein complex (Iqgap1) kinase activity (Kdr)
Kdr (Mus musculus)
Iqgap1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 60 97.76 Very High Very High Very High
ischemia 66 75.04 Quite High
Inflammatory response 2 70.16 Quite High
cytokine 6 35.16 Quite Low
chemokine 2 11.40 Low Low
fibrosis 6 5.00 Very Low Very Low Very Low
ketamine 2 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 62 97.76 Very High Very High Very High
Adhesions 22 92.92 High High
Injury 12 79.28 Quite High
Disease 4 76.12 Quite High
Cv Unclassified Under Development 66 75.04 Quite High
Vasculitis 2 64.56 Quite High
Cancer 6 40.08 Quite Low
Necrosis 22 39.64 Quite Low
Cardiovascular Disease 2 18.48 Low Low
Peritonitis 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We previously demonstrated that IQGAP1 directly binds to VEGFR2 [18] and it plays a critical role in transmitting VEGF-mediated signals to the angiogenesis-related responses in ECs [18], [19].
VEGFR2 Binding (binds) of IQGAP1
1) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.40 Pain Relevance 0.13
We and others have previously demonstrated that IQGAP1 directly binds to VEGFR2 or cSrc and B-Raf, and knockdown of endogenous IQGAP1 with siRNA inhibits VEGF-induced angiogenic responses in cultured ECs [18], [19], [20].
VEGFR2 Binding (binds) of IQGAP1
2) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.58 Pain Relevance 0.15

General Comments

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