INT243418

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Context Info
Confidence 0.30
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 14
Total Number 17
Disease Relevance 5.94
Pain Relevance 0.44

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 2
tibialis anterior 1
vesicle 1
Htt (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 72 98.00 Very High Very High Very High
cerebral cortex 50 94.00 High High
carbamazepine 1 81.16 Quite High
Thalamus 6 76.12 Quite High
Pyramidal cell 24 72.88 Quite High
depression 6 70.12 Quite High
nMDA receptor 37 50.08 Quite High
Inflammatory response 18 50.00 Quite Low
Glutamate receptor 6 36.68 Quite Low
Enkephalin 7 28.56 Quite Low
Disease Link Frequency Relevance Heat
Disease 506 100.00 Very High Very High Very High
Toxicity 134 99.80 Very High Very High Very High
Neurodegenerative Disease 89 99.60 Very High Very High Very High
Targeted Disruption 296 96.96 Very High Very High Very High
Stress 39 95.68 Very High Very High Very High
Epilepsy 3 95.04 Very High Very High Very High
Apoptosis 76 91.32 High High
Infection 40 83.36 Quite High
Dyskinesias 6 81.12 Quite High
Death 88 76.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The decrease of Ku70 was blocked by the protease inhibitor MG132 (Fig. 6 D), indicating that one part of the Ku70 and mutant Htt complex was degraded by the proteasome system, whereas another part forms intracellular aggregates.
mutant Htt Binding (complex) of
1) Confidence 0.30 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.08 Pain Relevance 0
Our experiments show that impairment of DNA repair through the interaction between Ku70 and mutant Htt accelerates accumulation of DSBs and causes neuronal dysfunction from an early stage of the HD pathology.
mutant Htt Binding (interaction) of in neuronal associated with disease
2) Confidence 0.30 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.80 Pain Relevance 0
S2 shows interaction between Ku70 and full-length mutant Htt protein.
mutant Htt Binding (interaction) of
3) Confidence 0.29 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.25 Pain Relevance 0
Altogether, the functional defect of Ku70 seems to be directly induced by interaction with mutant Htt rather than indirectly by sequestration or acetylation of Ku70.


mutant Htt Binding (interaction) of
4) Confidence 0.29 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.18 Pain Relevance 0
The interaction was observed with the construct 120–608 but not with 224–608, indicating that the mutant Htt exon 1 peptide interacts with the 120–223 region of the N-terminal domain.
mutant Htt Binding (interacts) of
5) Confidence 0.29 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0.03
Although coprecipitation of Ku70 and mutant Htt was observed with anti-polyQ and -Htt antibodies (1C2 and HD1), an interaction with wild-type Htt was not detected.
wild-type Htt Binding (interaction) of
6) Confidence 0.29 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0.05
The protein encoded by the HD gene, htt (huntingtin), is normally a cytoplasmic protein closely associated with vesicle membranes and microtubules.
HD Binding (associated) of in vesicle
7) Confidence 0.16 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2850512 Disease Relevance 0.77 Pain Relevance 0.14
HD genotyping
HD Binding (genotyping) of associated with disease
8) Confidence 0.16 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2865373 Disease Relevance 0.84 Pain Relevance 0
BAC models also have been instrumental in demonstrating an important role of cell–cell interactions, compared with cell autonomous processes, in HD pathogenesis (Gu et al., 2005, 2007; Gray et al., 2008a).
HD Binding (interactions) of
9) Confidence 0.14 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2850512 Disease Relevance 0.34 Pain Relevance 0
Another area that has not been extensively investigated is the function of glial cells and glio-neuronal interactions in HD.
HD Binding (interactions) of in neuronal
10) Confidence 0.14 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2850512 Disease Relevance 0.13 Pain Relevance 0.19
First of all, BC metabolism in humans is highly variable [16, 17] and most of this variability can be attributed to differences in enzymatic activity of the beta-carotene 15,15?
15,15 Binding (activity) of
11) Confidence 0.09 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2877315 Disease Relevance 0.51 Pain Relevance 0
(A) Cross-sections of mouse tibialis anterior muscle electroporated with GFP or huntingtin exon 1 with 23, 41, 74Q fused to GFP (Htt23Q, Htt41Q, Ht74Q).
huntingtin Binding (exon) of in tibialis anterior
12) Confidence 0.06 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2972693 Disease Relevance 0.15 Pain Relevance 0
Similar interactions among other heterogeneous proteins such as prion protein, huntingtin, A-Bri, and tau might be at play in other disorders of protein misfolding.


huntingtin Binding (interactions) of
13) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2519786 Disease Relevance 0.43 Pain Relevance 0
(C) Effect of PSA knockdown on aggregation of htt-exon-1-GFP with a polyglutamine repeat length of 23 was measured, exactly as in (A); data are shown normalized to control.
htt-exon-1-GFP Binding (aggregation) of
14) Confidence 0.06 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2972693 Disease Relevance 0.50 Pain Relevance 0
Thus, a decrease of only 50% in the endogenous PSA activity is sufficient to significantly enhance mutant huntingtin aggregate formation, as was also found upon treatment of 293A cells with PSA inhibitors.
huntingtin Binding (formation) of
15) Confidence 0.05 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2972693 Disease Relevance 0.17 Pain Relevance 0
PSA suppresses accumulation of mutant huntingtin aggregates and toxicity in vivo
huntingtin Binding (aggregates) of associated with toxicity
16) Confidence 0.05 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2972693 Disease Relevance 0.16 Pain Relevance 0
Another compound, trehalose, inhibits aggregation of mutant huntingtin and reduces toxicity in cells, and alleviates disease pathology in an HD mouse model [75].
huntingtin Binding (aggregation) of associated with toxicity and disease
17) Confidence 0.04 Published 2010 Journal Seminars in Cell & Developmental Biology Section Body Doc Link PMC2938570 Disease Relevance 0.64 Pain Relevance 0.04

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