INT346375

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Context Info
Confidence 0.33
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 11
Disease Relevance 1.56
Pain Relevance 2.46

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

vesicle-mediated transport (Vamp2) plasma membrane (Vamp2) protein complex assembly (Vamp2)
Anatomy Link Frequency
cleavage 7
neurons 4
Vamp2 (Mus musculus)
Pain Link Frequency Relevance Heat
tetrodotoxin 154 99.72 Very High Very High Very High
Action potential 55 99.00 Very High Very High Very High
Spinal cord 506 98.34 Very High Very High Very High
Central nervous system 66 90.76 High High
Neurotransmitter 44 75.48 Quite High
Calcium channel 11 37.76 Quite Low
imagery 11 19.68 Low Low
antagonist 33 5.00 Very Low Very Low Very Low
sodium channel 11 5.00 Very Low Very Low Very Low
nMDA receptor antagonist 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Anaerobic Bacterial Infections 242 99.34 Very High Very High Very High
Targeted Disruption 66 98.28 Very High Very High Very High
Infection 44 97.72 Very High Very High Very High
Disease 66 78.00 Quite High
Paralysis 77 72.96 Quite High
Poisoning 22 71.56 Quite High
Toxicity 11 67.12 Quite High
Trismus 11 25.00 Low Low
Injury 22 5.00 Very Low Very Low Very Low
Death 11 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As shown in Figure 3A, neurons that expressed the K44A mutant were protected from the entry of TeNT, as evidenced by the lack of cleavage of syb II, as compared to neurons that expressed WT dynamin.
Protein_catabolism (cleavage) of syb II in neurons
1) Confidence 0.33 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0 Pain Relevance 0.22
We titrated BoNT/F from 0.3 to 10 nM on WT and knockout neurons and observed no significant difference in binding and entry, as evidenced by cleavage of syb II, between these two conditions (Figure 5G).
Protein_catabolism (cleavage) of syb II in cleavage associated with targeted disruption
2) Confidence 0.33 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.17 Pain Relevance 0.07
As BoNT/A and BoNT/E cleave SNAP-25 instead of syb II, we were able to inhibit exocytosis in neurons while still monitor the entry of TeNT through cleavage of syb II.
Protein_catabolism (cleave) of syb II in cleavage
3) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0 Pain Relevance 0.16
We began by comparing the ability of TeNT to cleave syb II under TTX (which blocks action potentials to inhibit SV recycling) or high potassium (which depolarizes neurons to drive SV recycling) conditions.
Protein_catabolism (cleave) of syb II in neurons associated with action potential and tetrodotoxin
4) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.05 Pain Relevance 0.44
Furthermore, double KO neurons were largely protected from TeNT, as evidenced by the lack of cleavage of syb II; moreover, these neurons could be re-sensitized through infection with viruses that expressed SV2A or B.
Protein_catabolism (cleavage) of syb II in cleavage associated with infection
5) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.10 Pain Relevance 0.04
Hence, we first pre-treated spinal cord neurons with BoNT/A to cleave SNAP-25 and inhibit exocytosis [1], and then we subsequently assayed for entry of TeNT by monitoring cleavage of syb II.
Protein_catabolism (cleavage) of syb II in cleavage associated with spinal cord
6) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.07 Pain Relevance 0.07
Moreover, tetanus neurotoxin entry and subsequent cleavage of synaptobrevin II, the substrate for this toxin, was also dependent on synaptic vesicle recycling.
Protein_catabolism (cleavage) of synaptobrevin II in cleavage associated with anaerobic bacterial infections
7) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Abstract Doc Link PMC2991259 Disease Relevance 0.91 Pain Relevance 0.20
Because neuronal activity and SV recycling were required for the cleavage of syb II, indicating that the toxin receptor resided on SVs, we began to screen SV proteins for TeNT binding activity.
Protein_catabolism (cleavage) of syb II in cleavage
8) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0 Pain Relevance 0.21
Cleavage of synaptobrevin II is dependent on synaptic vesicle recycling
Protein_catabolism (Cleavage) of synaptobrevin II in Cleavage
9) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.08 Pain Relevance 0.53
Indeed, in hippocampal neurons, as well as in inhibitory spinal cord neurons that are the physiological targets of TeNT, we observed markedly enhanced cleavage of TeNT's substrate, syb II, under conditions that stimulate SV exo- and endocytosis.
Protein_catabolism (cleavage) of syb II in neurons associated with spinal cord
10) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.13 Pain Relevance 0.13
To test this idea, we determined whether the ability of TeNT holotoxin to enter neurons and cleave syb II also depended on SV recycling.
Protein_catabolism (cleave) of syb II in neurons
11) Confidence 0.22 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2991259 Disease Relevance 0.06 Pain Relevance 0.38

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