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Context Info
Confidence 0.04
First Reported 1991
Last Reported 2009
Negated 1
Speculated 0
Reported most in Abstract
Documents 2
Total Number 2
Disease Relevance 0.56
Pain Relevance 0.43

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

cell proliferation (Irs2) cytosol (Irs2) plasma membrane (Irs2)
cellular_component (Irs2)
Anatomy Link Frequency
chromaffin cells 1
Irs2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Catecholamine 1 98.46 Very High Very High Very High
Calcium channel 1 97.96 Very High Very High Very High
tetrodotoxin 1 97.92 Very High Very High Very High
sodium channel 1 97.06 Very High Very High Very High
Nav1.7 1 96.76 Very High Very High Very High
ischemia 1 85.32 High High
Inflammation 1 82.72 Quite High
Disease Link Frequency Relevance Heat
Cv Unclassified Under Development 1 85.32 High High
Neurodegenerative Disease 1 84.92 Quite High
INFLAMMATION 1 82.72 Quite High
Diabetes Mellitus 1 82.16 Quite High
Disease 2 77.00 Quite High
Attention Deficit Hyperactivity Disorder 1 75.20 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The K+ channel blocker tetraethylammonium did not modify K(+)-evoked release of Ps4 and Ps5.
Neg (not) Regulation (modify) of Ps4
1) Confidence 0.04 Published 1991 Journal Neuroscience Section Abstract Doc Link 1722891 Disease Relevance 0 Pain Relevance 0.10
In adrenal chromaffin cells, GSK-3 inhibition caused up-regulation of voltage-dependent Nav1.7 sodium channel, enhancing voltage-dependent calcium channel gating and catecholamine exocytosis; conversely, chronic treatment with GSK-3 inhibitors caused down-regulation of insulin receptor, IRS-1, IRS-2, and Akt1 levels.
Regulation (regulation) of IRS-2 in chromaffin cells associated with catecholamine, calcium channel, sodium channel and nav1.7
2) Confidence 0.03 Published 2009 Journal Front. Biosci. Section Abstract Doc Link 19273146 Disease Relevance 0.56 Pain Relevance 0.33

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