INT114136

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Context Info
Confidence 0.47
First Reported 2004
Last Reported 2010
Negated 0
Speculated 1
Reported most in Abstract
Documents 3
Total Number 5
Disease Relevance 2.02
Pain Relevance 0.97

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

transport (Vdac1) mitochondrion (Vdac1) plasma membrane (Vdac1)
protein complex (Vdac1) transmembrane transport (Vdac1)
Anatomy Link Frequency
neuronal 1
pore 1
Vdac1 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 18 99.24 Very High Very High Very High
anesthesia 12 97.36 Very High Very High Very High
Inflammatory response 26 60.48 Quite High
Inflammation 66 28.28 Quite Low
addiction 3 5.00 Very Low Very Low Very Low
fluoxetine 2 5.00 Very Low Very Low Very Low
isoflurane 2 5.00 Very Low Very Low Very Low
cva 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Death 91 99.00 Very High Very High Very High
Apoptosis 51 98.70 Very High Very High Very High
Targeted Disruption 5 92.56 High High
Influenza Virus Infection 52 90.24 High High
Sprains And Strains 148 86.76 High High
Disease 21 77.48 Quite High
Stress 3 68.80 Quite High
Infection 38 62.36 Quite High
INFLAMMATION 84 60.08 Quite High
Neurodegenerative Disease 5 57.40 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These data indicate that neuroactive steroid binding to VDAC-1, -2, or -3 is unlikely to mediate GABA(A) receptor modulation or anesthesia.
VDAC-1 Binding (binding) of associated with anesthesia and gaba
1) Confidence 0.47 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14593090 Disease Relevance 0 Pain Relevance 0.55
Antisera to VDAC-1 were shown to coimmunoprecipitate GABA(A) receptors, suggesting a functional relationship between steroid binding to VDAC-1 and modulation of GABA(A) receptor function.
VDAC-1 Binding (binding) of associated with gaba
2) Confidence 0.35 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14593090 Disease Relevance 0 Pain Relevance 0.38
It has been suggested that PB1-F2 is able to induce cell death by disrupting mitochondrial organization through interaction with inner mitochondrial membrane adenine nucleotide translocator 3 (ANT3) and the outer mitochondrial membrane voltage channel 1 (VDAC1) to produce a mitochondrial permeability transition [12].
VDAC1 Binding (interaction) of associated with death
3) Confidence 0.16 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2908617 Disease Relevance 1.00 Pain Relevance 0
Since its discovery the consensus has been that the PB1-F2 proteins from selected viruses are pro-apoptotic, targeting the mitochondria and inducing pore formation through association with VDAC1 and ANT3 [4], [11], [12], [19], [24].
VDAC1 Binding (association) of in pore associated with apoptosis
4) Confidence 0.16 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2908617 Disease Relevance 0.71 Pain Relevance 0.03
Our study suggests a link between transcriptional dysfunction and cell death in trinucleotide repeat mediated neuronal dysfunction through voltage dependent anion channel, Vdac1, which has been recently recognized as a critical determinant of cell death.



Vdac1 Spec (determinant) Binding (recognized) of in neuronal associated with death
5) Confidence 0.05 Published 2007 Journal PLoS ONE Section Abstract Doc Link PMC2064964 Disease Relevance 0.31 Pain Relevance 0

General Comments

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