INT287204

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Context Info
Confidence 0.99
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 2.80
Pain Relevance 0.53

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

Golgi apparatus (Htt) endoplasmic reticulum (Htt) mitochondrion organization (Htt)
embryo development (Htt) protein complex (Htt) cytoplasm (Htt)
Anatomy Link Frequency
neuronal 1
Htt (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 48 98.96 Very High Very High Very High
cerebral cortex 8 64.36 Quite High
Central nervous system 9 60.44 Quite High
Neurotransmitter 4 50.56 Quite High
Hippocampus 4 19.04 Low Low
Enkephalin 3 12.32 Low Low
nMDA receptor 25 5.00 Very Low Very Low Very Low
Pyramidal cell 16 5.00 Very Low Very Low Very Low
medulla 10 5.00 Very Low Very Low Very Low
Clonidine 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Frailty 30 95.92 Very High Very High Very High
Disease 267 89.96 High High
Weight Loss 30 88.96 High High
Toxicity 33 83.12 Quite High
Dementia 2 63.16 Quite High
Neurodegenerative Disease 23 60.88 Quite High
Neuropathic Pain 4 51.72 Quite High
Targeted Disruption 103 50.00 Quite Low
Muscle Disease 8 46.16 Quite Low
Muscular Atrophy 6 18.48 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Additional factors that might influence the propensity to form inclusions in a particular cell type could include expression level of the R6/2 transcript or Hdh gene, Htt proteolysis and protein folding and clearance networks.
Protein_catabolism (proteolysis) of Htt
1) Confidence 0.99 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2778556 Disease Relevance 0.81 Pain Relevance 0.06
Additional factors that might influence the propensity to form inclusions in a particular cell type could include expression level of the R6/2 transcript or Hdh gene, Htt proteolysis and protein folding and clearance networks.
Protein_catabolism (proteolysis) of Hdh
2) Confidence 0.88 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2778556 Disease Relevance 0.81 Pain Relevance 0.06
Proteolysis of mutant huntingtin releases a persistent N-terminal fragment comprising the first 100–150 residues with the expanded polyglutamine sequence.
Protein_catabolism (Proteolysis) of mutant huntingtin
3) Confidence 0.43 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2865373 Disease Relevance 0.97 Pain Relevance 0
Perhaps these differences in glutamate release make striatal D2 cells more susceptible to degeneration in HD.


Protein_catabolism (degeneration) of HD associated with glutamate
4) Confidence 0.34 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2850512 Disease Relevance 0.07 Pain Relevance 0.19
How do the electrophysiological findings reviewed here contribute to our understanding of neuronal dysfunction and degeneration in HD?
Protein_catabolism (degeneration) of HD in neuronal
5) Confidence 0.34 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2850512 Disease Relevance 0.09 Pain Relevance 0.22
Consequently, in degrading huntingtin, the 26S proteasome appears to release polyglutamine-rich fragments for digestion by cytosolic peptidases (6,7).
Protein_catabolism (degrading) of huntingtin
6) Confidence 0.15 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2972693 Disease Relevance 0.05 Pain Relevance 0

General Comments

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