INT68695

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Context Info
Confidence 0.77
First Reported 1997
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 63
Total Number 64
Disease Relevance 44.54
Pain Relevance 3.69

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) protein complex (HTT)
cytoplasm (HTT) cytosol (HTT) cell death (HTT)
Anatomy Link Frequency
neurons 7
Skin 4
brain 3
interneurons 3
neuronal 3
HTT (Homo sapiens)
Pain Link Frequency Relevance Heat
Serotonin 17 100.00 Very High Very High Very High
methotrexate 2 99.12 Very High Very High Very High
Pain management 16 98.98 Very High Very High Very High
Glutamate 100 97.26 Very High Very High Very High
Pain 181 97.08 Very High Very High Very High
ischemia 18 96.20 Very High Very High Very High
Dopamine 51 94.32 High High
Cannabinoid 9 92.72 High High
hyperexcitability 16 92.28 High High
positron emission tomography 1 92.00 High High
Disease Link Frequency Relevance Heat
Disease 1198 100.00 Very High Very High Very High
Alzheimer's Dementia 48 100.00 Very High Very High Very High
Epstein-barr Virus 18 100.00 Very High Very High Very High
Huntington's Chorea 12 100.00 Very High Very High Very High
Wound Healing 606 99.92 Very High Very High Very High
Death 218 99.80 Very High Very High Very High
Lifespan 52 99.80 Very High Very High Very High
Toxicity 629 99.76 Very High Very High Very High
Blister 1054 99.68 Very High Very High Very High
Intellectual Impairment 5 99.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Combined techniques for NADPH-diaphorase enzyme histochemistry and huntingtin immunocytochemistry, as well as double immunofluorescence for either nitric oxide synthase or calbindin D28k in comparison with huntingtin expression, revealed a striking correspondence between calbindin D28k and huntingtin immunoreactivities, with little or no colocalization between NADPH-diaphorase or nitric oxide synthase neurons and huntingtin expression.
Gene_expression (expression) of huntingtin in neurons
1) Confidence 0.77 Published 1997 Journal J. Neurosci. Section Abstract Doc Link 9096140 Disease Relevance 0.09 Pain Relevance 0.06
Heterogeneous topographic and cellular distribution of huntingtin expression in the normal human neostriatum.
Gene_expression (expression) of huntingtin
2) Confidence 0.77 Published 1997 Journal J. Neurosci. Section Title Doc Link 9096140 Disease Relevance 0 Pain Relevance 0.08
These observations suggest that the selective vulnerability of spiny striatal neurons and the matrix compartment observed in Huntington's disease is associated with higher levels of huntingtin expression, whereas the relative resistance of large and medium-sized aspiny neurons and the patch compartments to degeneration is associated with low levels of huntingtin expression.
Gene_expression (expression) of huntingtin in neurons associated with disease
3) Confidence 0.77 Published 1997 Journal J. Neurosci. Section Abstract Doc Link 9096140 Disease Relevance 0.10 Pain Relevance 0.05
Combined techniques for NADPH-diaphorase enzyme histochemistry and huntingtin immunocytochemistry, as well as double immunofluorescence for either nitric oxide synthase or calbindin D28k in comparison with huntingtin expression, revealed a striking correspondence between calbindin D28k and huntingtin immunoreactivities, with little or no colocalization between NADPH-diaphorase or nitric oxide synthase neurons and huntingtin expression.
Gene_expression (expression) of huntingtin in neurons
4) Confidence 0.77 Published 1997 Journal J. Neurosci. Section Abstract Doc Link 9096140 Disease Relevance 0.07 Pain Relevance 0.07
These observations suggest that the selective vulnerability of spiny striatal neurons and the matrix compartment observed in Huntington's disease is associated with higher levels of huntingtin expression, whereas the relative resistance of large and medium-sized aspiny neurons and the patch compartments to degeneration is associated with low levels of huntingtin expression.
Gene_expression (expression) of huntingtin in neurons associated with disease
5) Confidence 0.77 Published 1997 Journal J. Neurosci. Section Abstract Doc Link 9096140 Disease Relevance 0.10 Pain Relevance 0
The stable inducible PC12 cells have been previously described (11), cells were treated with doxycycline to induce huntingtin expression for 24 h at 1 µg/ml with the addition of 1 µm rilmenidine for a further 24 h and bafilomycin A1 as for primary neurons.


Gene_expression (expression) of huntingtin in primary neurons
6) Confidence 0.75 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2865373 Disease Relevance 0 Pain Relevance 0
In the cortical model, we showed expression of mhtt-exon1 in CPNs resulted in mild degenerative changes (i.e. dark degenerating vacuoles in the CPNs under EM; see ref. [27]); and in the striatal model, electrophysiological recordings revealed cell-autonomous NMDA receptor-mediated response changes in dissociated MSNs.
Gene_expression (expression) of htt associated with nmda receptor
7) Confidence 0.75 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC1885431 Disease Relevance 0.53 Pain Relevance 0.07
To further determine the specificity and extent of mhtt-exon1 expression in MSNs in the striatal, cortical and pan-neuronal models of HD, we performed double immunofluorescent staining using EM48 and Darpp-32, a marker for striatal MSNs in 6 month old mice [30].
Gene_expression (expression) of htt in neuronal associated with disease
8) Confidence 0.75 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC1885431 Disease Relevance 0.38 Pain Relevance 0.03
For example, selective expression of mhtt-exon1 in CPNs is not sufficient to cause a significant striatal phenotype in the cortical model.
Gene_expression (expression) of htt
9) Confidence 0.75 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC1885431 Disease Relevance 0.76 Pain Relevance 0.05
Since striatal expression of mhtt-exon1 is comparable in the two models driven by the same endogenous Rosa26 promoter, as demonstrated by EM48 nuclear accumulation in MSNs, our results clearly demonstrate that cell-autonomous toxicity of mhtt in striatal MSNs is not sufficient to elicit robust motor deficits and striatal neuropathology in these mice.
Gene_expression (expression) of htt associated with toxicity
10) Confidence 0.75 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC1885431 Disease Relevance 0.62 Pain Relevance 0.08
Interestingly, glutamate uptake inhibition in the rat striatum has been shown to trigger massive neuronal loss [35] mimicking excitotoxic HD models [3], and the expression of a mutant form of huntingtin decreases GLT-1 expression in transgenic HD mice [36] and in patients [34].
Gene_expression (expression) of huntingtin in neuronal associated with targeted disruption, glutamate and disease
11) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2798716 Disease Relevance 0.95 Pain Relevance 0.32
Here, we report that in vitro models of disease comprised of primary striatal neurons expressing N-terminal fragments of mutant huntingtin (via lentiviral gene delivery) faithfully reproduce the gene expression changes seen in human HD.
Gene_expression (expressing) of huntingtin in neurons associated with disease
12) Confidence 0.75 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18815258 Disease Relevance 0.62 Pain Relevance 0
HD-related transcriptomic changes were also observed in primary neurons expressing a longer fragment of mutant huntingtin (htt853-82Q).
Gene_expression (expressing) of huntingtin in primary neurons associated with disease
13) Confidence 0.75 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18815258 Disease Relevance 0.67 Pain Relevance 0.14
Expression of a wild-type fragment of huntingtin [htt171-18Q] also caused only a small number of RNA changes.
Gene_expression (Expression) of huntingtin
14) Confidence 0.75 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18815258 Disease Relevance 0.74 Pain Relevance 0.03
We have shown that mutant huntingtin fragments, expanded polyalanines tagged with GFP, and mutant forms of ?
Gene_expression (fragments) of huntingtin
15) Confidence 0.65 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2856980 Disease Relevance 0.34 Pain Relevance 0
The gene product huntingtin is widely distributed in both neurones and extraneuronal tissues.
Gene_expression (distributed) of huntingtin
16) Confidence 0.65 Published 2004 Journal J Neural Transm Section Abstract Doc Link 15480847 Disease Relevance 0.52 Pain Relevance 0
Lithium chloride treatment reduced toxicity induced by overexpression of Huntington disease exon 1 fragment with 74 glutamines in neuronal and non-neuronal cell lines [11], and attenuated toxicity of the N-terminal part of mutant huntingtin with 120 glutamine repeats in Drosophila [39].
Gene_expression (overexpression) of Huntington disease in neuronal associated with toxicity and huntington's chorea
17) Confidence 0.65 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 1.23 Pain Relevance 0.03
(A) PSA expression levels alter lifespan in flies expressing htt-exon1 with 93 polyglutamine repeats in the brain.
Gene_expression (expressing) of htt in brain associated with lifespan
18) Confidence 0.65 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2972693 Disease Relevance 0.70 Pain Relevance 0
HD is caused by a trinucleotide expansion in the IT15 gene, coding for the mutant protein huntingtin, and has an autosomal dominant hereditary pattern.
Gene_expression (expansion) of huntingtin associated with disease
19) Confidence 0.65 Published 2010 Journal Curr Treat Options Neurol Section Body Doc Link PMC2918785 Disease Relevance 1.06 Pain Relevance 0.08
To begin to experimentally address this issue we have developed a Cre/LoxP conditional mouse model of HD (termed RosaHD mice) in which expression of a neuropathogenic fragment of mhtt (mhtt-exon1), driven by the endogenous ubiquitously-expressing Rosa26 promoter, can be switched on by Cre recombinase (Fig. 1A; also ref. [27]).
Gene_expression (expression) of htt associated with disease
20) Confidence 0.58 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC1885431 Disease Relevance 0.64 Pain Relevance 0.08

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