INT240719

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Context Info
Confidence 0.08
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 7
Disease Relevance 2.33
Pain Relevance 0.04

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

mitochondrion (ATP6) aging (ATP6) ATPase activity (ATP6)
molecular_function (ATP6) cellular_component (ATP6)
Anatomy Link Frequency
muscle 3
respiratory 2
sensory neurons 1
ATP6 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 3 71.08 Quite High
ischemia 16 5.00 Very Low Very Low Very Low
qutenza 11 5.00 Very Low Very Low Very Low
Glutamate 6 5.00 Very Low Very Low Very Low
imagery 6 5.00 Very Low Very Low Very Low
Calcitonin gene-related peptide 5 5.00 Very Low Very Low Very Low
cytokine 3 5.00 Very Low Very Low Very Low
Central nervous system 3 5.00 Very Low Very Low Very Low
anesthesia 3 5.00 Very Low Very Low Very Low
substance P 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Paralysis 21 99.84 Very High Very High Very High
Muscle Weakness 45 98.64 Very High Very High Very High
Targeted Disruption 3 98.52 Very High Very High Very High
Poisoning 78 97.88 Very High Very High Very High
Hypoxia 149 93.28 High High
Emergencies 3 92.80 High High
Stress 66 83.32 Quite High
Body Weight 9 57.20 Quite High
Toxicity 12 12.92 Low Low
Cv Unclassified Under Development 14 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In conclusion, the studies demonstrate that muscle mitochondrial ATP synthase is inhibited in paralyzed muscle during the early phase of acute monocrotophos exposure, an effect possibly mediated through NO.
Negative_regulation (inhibited) of mitochondrial ATP synthase in muscle associated with paralysis
1) Confidence 0.08 Published 2009 Journal Toxicology Mechanisms and Methods Section Body Doc Link PMC2736536 Disease Relevance 0.33 Pain Relevance 0
Mitochondrial ATP synthase inhibition and nitric oxide are involved in muscle weakness that occurs in acute exposure of rats to monocrotophos

Organophosphate poisoning in the context of self-harm is a common medical emergency in Asia.

Negative_regulation (inhibition) of Mitochondrial ATP synthase in muscle associated with emergencies, muscle weakness and poisoning
2) Confidence 0.06 Published 2009 Journal Toxicology Mechanisms and Methods Section Title Doc Link PMC2736536 Disease Relevance 0.61 Pain Relevance 0
Muscle mitochondrial ATP synthase activity was inhibited in the rat in acute exposure to monocrotophos while respiration per se was not affected.
Negative_regulation (inhibited) of mitochondrial ATP synthase in Muscle
3) Confidence 0.06 Published 2009 Journal Toxicology Mechanisms and Methods Section Abstract Doc Link PMC2736536 Disease Relevance 0.59 Pain Relevance 0
We note that oligomycin, an inhibitor of mitochondrial ATP synthase, has recently been reported to change the dynamics of caffeine-induced Ca2+ oscillations in sensory neurons.
Negative_regulation (inhibitor) of mitochondrial ATP synthase in sensory neurons
4) Confidence 0.02 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.39 Pain Relevance 0
In summary, the use of WT and RG cells allows us to distinguish several different mechanisms by which AMPK can be activated, of which the first three cause indirect activation by increasing cellular AMP: (1) inhibition of the respiratory chain (biguanides, galegine, troglitazone, phenobarbital, berberine), (2) inhibition of the mitochondrial ATP synthase (oligomycin, resveratrol), (3) inhibition of glycolysis (2-deoxyglucose), (4) increasing cytoplasmic Ca2+ (A23187), (5) intracellular conversion into an AMP mimetic (AICAR), and (6) direct binding to AMPK at a site distinct from the AMP site (A769662).
Negative_regulation (inhibition) of mitochondrial ATP synthase in respiratory
5) Confidence 0.01 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2935965 Disease Relevance 0.16 Pain Relevance 0
Resveratrol inhibits the mitochondrial ATP synthase (Zheng and Ramirez, 2000) by binding to the ?
Negative_regulation (inhibits) of mitochondrial ATP synthase
6) Confidence 0.01 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2935965 Disease Relevance 0.10 Pain Relevance 0.04
In summary, the use of WT and RG cells allows us to distinguish several different mechanisms by which AMPK can be activated, of which the first three cause indirect activation by increasing cellular AMP: (1) inhibition of the respiratory chain (biguanides, galegine, troglitazone, phenobarbital, berberine), (2) inhibition of the mitochondrial ATP synthase (oligomycin, resveratrol), (3) inhibition of glycolysis (2-deoxyglucose), (4) increasing cytoplasmic Ca2+ (A23187), (5) intracellular conversion into an AMP mimetic (AICAR), and (6) direct binding to AMPK at a site distinct from the AMP site (A769662).
Negative_regulation (inhibition) of mitochondrial ATP synthase in respiratory
7) Confidence 0.01 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2935965 Disease Relevance 0.16 Pain Relevance 0

General Comments

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