INT257320

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Context Info
Confidence 0.22
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.58
Pain Relevance 0

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

endosome (Nox1) signal transduction (Nox1) transport (Nox1)
oxidoreductase activity (Nox1) plasma membrane (Nox1) extracellular matrix organization (Nox1)
Anatomy Link Frequency
smooth muscle 2
Nox1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
fibrosis 2 47.48 Quite Low
Inflammation 4 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
antagonist 2 5.00 Very Low Very Low Very Low
ketamine 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 1 95.80 Very High Very High Very High
Hypertension 14 95.64 Very High Very High Very High
Stroke 1 91.08 High High
Hypertrophy 5 90.28 High High
Stress 8 54.44 Quite High
Cardiovascular Disorder Under Development 4 50.00 Quite Low
Fibrosis 3 47.48 Quite Low
Coronary Heart Disease 3 46.96 Quite Low
Cancer 1 8.96 Low Low
Necrosis 1 8.48 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Although p22phox alone does not support superoxide production but it has been clearly shown to stabilize the expression of gp91phox (20) and Nox1 (21) in culture, probably serving as a stabilizing and/or regulatory subunit. p22phox overexpression in transgenic (Tg) mice (Tgp22smc) that overexpress the p22phox subunit of NAD(P)H oxidase selectively in smooth muscle, concomitantly upregulates Nox1, and potentates angiotensin II induced vascular hypertrophy (22).
Negative_regulation (stabilize) of Gene_expression (expression) of Nox1 in smooth muscle associated with targeted disruption and hypertrophy
1) Confidence 0.22 Published 2008 Journal Journal of Korean Medical Science Section Body Doc Link PMC2610641 Disease Relevance 0.58 Pain Relevance 0

General Comments

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