INT249183

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Context Info
Confidence 0.01
First Reported 2007
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.26
Pain Relevance 0.09

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

cytoplasm (ITPR3, GOPC) nucleoplasm (ITPR3) small molecule metabolic process (ITPR3)
Golgi apparatus (GOPC) endoplasmic reticulum (ITPR3) transmembrane transport (ITPR3)
Anatomy Link Frequency
plasma 1
ITPR3 (Homo sapiens)
GOPC (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 88 91.56 High High
cytokine 1 45.48 Quite Low
substance P 1 7.64 Low Low
Inflammation 8 5.00 Very Low Very Low Very Low
addiction 3 5.00 Very Low Very Low Very Low
TRP channel 2 5.00 Very Low Very Low Very Low
antagonist 2 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
b2 receptor 1 5.00 Very Low Very Low Very Low
Inflammatory mediators 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Adhesions 6 76.08 Quite High
INFLAMMATION 11 5.00 Very Low Very Low Very Low
Disease 5 5.00 Very Low Very Low Very Low
Stress 4 5.00 Very Low Very Low Very Low
Targeted Disruption 3 5.00 Very Low Very Low Very Low
Increased Venous Pressure Under Development 3 5.00 Very Low Very Low Very Low
Thrombosis 2 5.00 Very Low Very Low Very Low
Hypertension 2 5.00 Very Low Very Low Very Low
Neutrophil Disorders 2 5.00 Very Low Very Low Very Low
Asthma 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
S331A cells with U46619 impaired, but did not fully abolish [Ca2+]i mobilization and IP3 generation (Fig. 5D–F) in response to secondary stimulation with U46619.
IP3 Binding (generation) of Fig
1) Confidence 0.01 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.09
Three models have been put forward to link store-emptying to SOCs activation (reviewed by Putney et al. [46]): a dynamic, conformational coupling [41] (Fig. 1) involving a direct protein–protein interaction between InsP3-Rs and SOCs; an unidentified, diffusible messenger, termed calcium influx factor [33, 464748], generated and released in response to store depletion; and a fusion of secretory vesicles [49, 50] with the plasma membrane causing preformed SOCs protein insertion into the plasma membrane through exocytosis or regulatory molecules.
InsP3 Binding (interaction) of Fig in plasma
2) Confidence 0.01 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0.26 Pain Relevance 0

General Comments

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