INT26734

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Context Info
Confidence 0.29
First Reported 1987
Last Reported 2007
Negated 1
Speculated 0
Reported most in Abstract
Documents 4
Total Number 4
Disease Relevance 1.01
Pain Relevance 1.19

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

cytosol (Pdpk1) cytoplasmic membrane-bounded vesicle (Pdpk1) plasma membrane (Pdpk1)
nucleus (Pdpk1) kinase activity (Pdpk1) cytoplasm (Pdpk1)
Pdpk1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 7 100.00 Very High Very High Very High
hyperexcitability 5 98.76 Very High Very High Very High
Lasting pain 3 97.84 Very High Very High Very High
adenocard 1 93.64 High High
ischemia 42 84.04 Quite High
Inflammation 5 83.00 Quite High
Kinase C inhibitor 1 80.24 Quite High
anesthesia 2 79.20 Quite High
agonist 2 75.00 Quite High
Clonidine 1 74.08 Quite High
Disease Link Frequency Relevance Heat
Poisoning 1 100.00 Very High Very High Very High
Pain 3 97.84 Very High Very High Very High
Cv Unclassified Under Development 42 84.04 Quite High
INFLAMMATION 3 83.00 Quite High
Nervous System Injury 3 75.00 Quite High
Nociception 3 75.00 Quite High
Injury 13 56.08 Quite High
Neuropathic Pain 1 31.76 Quite Low
Death 1 20.48 Low Low
Spermatic Cord Torsion 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
They also establish the association between protein kinase G, the induction of long-term hyperexcitability, and chronic pain in rodents.
protein kinase Binding (association) of associated with lasting pain and hyperexcitability
1) Confidence 0.29 Published 2006 Journal Neuroscience Section Abstract Doc Link 16730916 Disease Relevance 0.56 Pain Relevance 0.41
Phenobarbital competes with diacylglycerol for protein kinase C.
protein kinase Binding (competes) of associated with kinase c
2) Confidence 0.23 Published 1987 Journal Life Sci. Section Title Doc Link 3796214 Disease Relevance 0 Pain Relevance 0.18
We conclude that (1) islet lipoxygenase is constitutively expressed and is not physiologically regulated by alpha 2-adrenergic agonism, Ca2+ or protein kinases; (2) lipoxygenase modulates insulin release; HETE production is not merely an epiphenomenon reflecting the activation (or inhibition) of exocytotic secretion; (3) islet lipoxygenase inhibitors reduce insulin secretion, at least in part, by blocking the direct effects of Ca2+ on exocytosis and/or its synergism with Ca2+-binding proteins such as protein kinase C; and (4) these same inhibitors do not directly poison protein kinase C or A, or the exocytotic apparatus.
protein kinase Neg (not) Binding (do) of associated with kinase c and poisoning
3) Confidence 0.03 Published 1989 Journal Biochem. Pharmacol. Section Abstract Doc Link 2567595 Disease Relevance 0.10 Pain Relevance 0.28
Cellular stressors activate protein kinase via G-protein-coupled receptor binding and membrane phospholipase activation.
protein kinase Binding (binding) of
4) Confidence 0.01 Published 2007 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2231361 Disease Relevance 0.35 Pain Relevance 0.33

General Comments

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