INT124246

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Context Info
Confidence 0.37
First Reported 2005
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 10
Total Number 12
Disease Relevance 6.53
Pain Relevance 0.90

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

cytosol (Snca) mitochondrion (Snca) histone binding (Snca)
plasma membrane (Snca) cytoskeleton (Snca) nucleus (Snca)
Anatomy Link Frequency
neurons 1
Snca (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 104 99.84 Very High Very High Very High
Substantia nigra 50 91.52 High High
monoamine 8 85.76 High High
Catecholamine 16 71.20 Quite High
Spinal cord 32 70.08 Quite High
Pain threshold 1 65.68 Quite High
Eae 8 54.00 Quite High
medulla 5 16.32 Low Low
Central nervous system 39 5.00 Very Low Very Low Very Low
Inflammation 17 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Parkinson's Disease 406 99.76 Very High Very High Very High
Stress 164 99.12 Very High Very High Very High
Anxiety Disorder 8 98.56 Very High Very High Very High
Sprains And Strains 5 97.72 Very High Very High Very High
Drug Induced Neurotoxicity 16 97.32 Very High Very High Very High
Toxicity 72 94.16 High High
Disease 801 92.04 High High
Targeted Disruption 100 91.12 High High
Gliosis 1 81.84 Quite High
Apoptosis 56 76.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To investigate whether alpha-synuclein was aggregated, we double stained with alpha-synuclein and Thioflavine-S, a marker for ?
alpha-synuclein Binding (marker) of
1) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.22 Pain Relevance 0.04
We show that alpha-syn does not account for differences in extinction in a fear conditioning task, as its expression did not covary with the decrease of freezing on repeated non-reinforced tone and context exposure in the three strains: B6Jax exhibited fastest extinction followed by B6JOla.
alpha-syn Neg (not) Binding (account) of associated with anxiety disorder and sprains and strains
2) Confidence 0.36 Published 2005 Journal Behav. Brain Res. Section Abstract Doc Link 15639180 Disease Relevance 0.93 Pain Relevance 0.07
Levels of SNCA protein have been found to increase upon exposure to oxidative stress [50], potentially through stabilization of SNCA by oxidative ligation to dopamine [19].
SNCA Binding (ligation) of associated with stress and dopamine
3) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.46 Pain Relevance 0.25
This susceptibility may be due to the increased tendency of SNCA to aggregate when exposed to oxidative stress [14]–[18], and the stabilization of a toxic protofibril form of SNCA by oxidative ligation of SNCA to dopamine [19].
SNCA Binding (ligation) of associated with stress and dopamine
4) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 1.50 Pain Relevance 0.32
Moreover, it seems that proteasomal dysfunction may potentiate alpha-synuclein oligomerization, which in turn can have an inhibitory effect on the proteasomal activities.
alpha-synuclein Binding (oligomerization) of
5) Confidence 0.26 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.26 Pain Relevance 0
Our recent results corroborate the notion that a mitochondrial dysfunction induces an oligomerization of alpha-synuclein (Esteves et al., 2010a).
alpha-synuclein Binding (oligomerization) of associated with parkinson's disease
6) Confidence 0.26 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.27 Pain Relevance 0
Alpha-synuclein exists in solution as an unfolded monomer but can easily aggregate and form insoluble antiparallel beta-sheet fibrillar oligomers (Moore et al., 2005).
Alpha-synuclein Binding (aggregate) of
7) Confidence 0.20 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.70 Pain Relevance 0.03
Moreover, it seems to be clear that alpha-synuclein interacts with tubulin, inhibiting microtubule formation and thus regulating microtubule dynamics in neurons (Zhou et al., 2009).
alpha-synuclein Spec (clear) Binding (interacts) of in neurons
8) Confidence 0.20 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.27 Pain Relevance 0.12
Recently, Gitler et al. (2009) reported a strong genetic interaction between alpha-synuclein and ATP13A2.
alpha-synuclein Binding (interaction) of
9) Confidence 0.20 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.58 Pain Relevance 0
Additionally, we proved that an increase in free/polymerized tubulin ratio may increase alpha-synuclein oligomerization when a mitochondrial dependent ATP depletion and reactive oxygen species (ROS) generation occurs (Esteves et al., 2009).
alpha-synuclein Binding (oligomerization) of
10) Confidence 0.19 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.29 Pain Relevance 0.03
Interestingly, tubulin can stimulate alpha-synuclein fibrils formation in yeast and it was proved that by inhibiting microtubule dynamics or deleting genes involved in microtubule biogenesis, alpha-synuclein aggregation and toxicity increased (Kim et al., 2008).
alpha-synuclein Binding (formation) of associated with toxicity
11) Confidence 0.17 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.32 Pain Relevance 0
These authors claim that mitochondrial compromise is the primary event followed by proteasome impairment and consequent alpha-synuclein aggregation.
alpha-synuclein Binding (aggregation) of
12) Confidence 0.17 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.72 Pain Relevance 0.06

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