INT161459

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Context Info
Confidence 0.20
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 0.60
Pain Relevance 1.82

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

transport (Napb) vesicle-mediated transport (Napb)
Anatomy Link Frequency
neurons 2
neuroendocrine cells 1
brain 1
Napb (Mus musculus)
Pain Link Frequency Relevance Heat
bradykinin 1 99.14 Very High Very High Very High
Action potential 34 98.30 Very High Very High Very High
Neurotransmitter 40 95.44 Very High Very High Very High
GABAergic 135 93.72 High High
Nerve growth factor 1 90.00 High High
Glutamate 72 86.68 High High
nociceptor 5 86.32 High High
antidepressant 26 85.44 High High
Inflammation 4 75.00 Quite High
Root ganglion neuron 1 74.32 Quite High
Disease Link Frequency Relevance Heat
Stress 110 82.04 Quite High
INFLAMMATION 3 75.00 Quite High
Ganglion Cysts 1 74.00 Quite High
Hyperalgesia 1 58.76 Quite High
Pain 1 54.44 Quite High
Urological Neuroanatomy 6 50.00 Quite Low
Convulsion 13 5.56 Low Low
Targeted Disruption 19 5.00 Very Low Very Low Very Low
Anxiety Disorder 8 5.00 Very Low Very Low Very Low
Cognitive Disorder 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, SNAP-25 is required for neurons to establish AP-evoked synchronous network activity, as measured by calcium transients, whereas the loss of this t-SNARE does not affect voltage-dependent calcium entry.



Negative_regulation (loss) of t-SNARE in neurons associated with action potential
1) Confidence 0.20 Published 2008 Journal BMC Neurosci Section Abstract Doc Link PMC2600647 Disease Relevance 0 Pain Relevance 0.33
For example, the analysis of neurons and neuroendocrine cells of SNAP-25 null mutant mice, generated by homologous recombination-mediated disruption of this t-SNARE gene [3], has demonstrated the selective abrogation of evoked neurotransmission, leaving constitutive release of neurotransmitter in catecholaminergic [4], GABAergic [5], glutamatergic and cholinergic systems [3] intact, despite varying effects on the amplitude and frequency of these transmitter-specific release events.
Negative_regulation (disruption) of t-SNARE in neurons associated with neurotransmitter and gabaergic
2) Confidence 0.20 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2600647 Disease Relevance 0 Pain Relevance 0.31
28 kDa (free SNAP-25) to higher molecular weight SNAP-25 containing complexes indicated that the stability of SNARE complexes was reduced in SNAP-25b deficient mouse brain.
Negative_regulation (reduced) of SNARE in brain
3) Confidence 0.12 Published 2008 Journal PLoS Genetics Section Body Doc Link PMC2581893 Disease Relevance 0 Pain Relevance 0
For example, the analysis of neurons and neuroendocrine cells of SNAP-25 null mutant mice, generated by homologous recombination-mediated disruption of this t-SNARE gene [3], has demonstrated the selective abrogation of evoked neurotransmission, leaving constitutive release of neurotransmitter in catecholaminergic [4], GABAergic [5], glutamatergic and cholinergic systems [3] intact, despite varying effects on the amplitude and frequency of these transmitter-specific release events.
Negative_regulation (disruption) of t-SNARE in neuroendocrine cells associated with neurotransmitter and gabaergic
4) Confidence 0.07 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2600647 Disease Relevance 0 Pain Relevance 0.31
The SNARE complex is SDS-resistant and can be visualized by loading in SDS-PAGE samples of purified presynaptic membranes treated at 25°C instead of 100°C, performing Western blot with antibody for syntaxin-1, and quantitating the complex by digital densitometry [24]–[26].
Negative_regulation (resistant) of SNARE
5) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797327 Disease Relevance 0.21 Pain Relevance 0.21
In contrast, TRPV1 sensitization caused by bradykinin, IL-1beta, and artemin was insensitive to inhibition of SNARE-dependent vesicular fusion and was not due to an increase in TRPV1 surface expression.
Negative_regulation (inhibition) of SNARE associated with bradykinin
6) Confidence 0.03 Published 2009 Journal FASEB J. Section Abstract Doc Link 19584302 Disease Relevance 0.40 Pain Relevance 0.65

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