INT309513

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Context Info
Confidence 0.30
First Reported 2010
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 18
Disease Relevance 3.69
Pain Relevance 0.21

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

protein complex (Xrcc6, Htt) cytoplasm (Xrcc6, Htt) nucleus (Xrcc6, Htt)
lyase activity (Xrcc6) Golgi apparatus (Htt) endoplasmic reticulum (Htt)
Anatomy Link Frequency
neurons 3
neuronal 1
HeLa 1
cerebral cortex 1
striatum 1
Xrcc6 (Mus musculus)
Htt (Mus musculus)
Pain Link Frequency Relevance Heat
cerebral cortex 108 98.80 Very High Very High Very High
imagery 36 5.00 Very Low Very Low Very Low
anesthesia 18 5.00 Very Low Very Low Very Low
Hippocampus 18 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 900 98.36 Very High Very High Very High
Stress 90 95.68 Very High Very High Very High
Targeted Disruption 594 93.96 High High
Lifespan 90 93.68 High High
Infection 90 90.16 High High
Dyskinesias 18 81.12 Quite High
Dna Damage 72 73.12 Quite High
Death 144 69.00 Quite High
Ataxia 18 56.72 Quite High
Aging 108 43.64 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Simultaneously, coprecipitation of Ku70 with Htt was tested.
Ku70 Binding (coprecipitation) of Htt
1) Confidence 0.30 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0
Immunocytochemistry of primary cortical neurons expressing mutant Htt also supported the association between Htt and Ku70 because mutant Htt and Ku70 were colocalized in inclusion bodies of primary cortical neurons (Fig. 4 A).
Ku70 Binding (association) of Htt in neurons
2) Confidence 0.29 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0
Immunocytochemistry of primary cortical neurons expressing mutant Htt also supported the association between Htt and Ku70 because mutant Htt and Ku70 were colocalized in inclusion bodies of primary cortical neurons (Fig. 4 A).
Ku70 Binding (association) of Htt in neurons
3) Confidence 0.29 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0
As mutant Htt interacts only with Ku70 among three components of the DNA–PK complex in IP assay (unpublished data), these results collectively suggest that the soluble form of mutant Htt directly disturbs the DNA–PK complex function through interaction with Ku70, which is consistent with the recent concept that soluble mutant Htt is toxic (Arrasate et al., 2004).
Ku70 Binding (interacts) of mutant Htt
4) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.09 Pain Relevance 0
These results suggest that impairment of DNA damage repair caused by the interaction between Ku70 and mutant Htt is a critical pathological component of HD.


Ku70 Binding (interaction) of mutant Htt associated with disease
5) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.68 Pain Relevance 0
S2 shows interaction between Ku70 and full-length mutant Htt protein.
Ku70 Binding (interaction) of mutant Htt
6) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.25 Pain Relevance 0
Mutant Htt interacts with Ku70, impairs DNA-dependent protein kinase function in nonhomologous end joining, and consequently increases DSB accumulation.
Ku70 Binding (interacts) of Mutant Htt
7) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Abstract Doc Link PMC2867301 Disease Relevance 0.41 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.
Ku70 Binding (interaction) of mutant Htt in neuronal associated with disease
8) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.80 Pain Relevance 0
Therefore, mutant Htt might impair NHEJ of DSBs by the DNA–PK complex through interaction with Ku70.
Ku70 Spec (might) Binding (interaction) of mutant Htt
9) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.19 Pain Relevance 0.04
These data collectively suggest that the shorter Htt exon 1 peptides, including the polyQ tract, do interact with Ku70 and that mutant Htt interacts with Ku70 more strongly than wild-type Htt.
Ku70 Binding (interacts) of mutant Htt
10) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0.04
Addressing these questions, we found that mutant Htt interacts with Ku70, functionally impairs Ku70-dependent DNA-dependent protein kinase (DNA–PK) activity for nonhomologous end joining (NHEJ) of DSBs in vitro and in vivo, and contributes to the accumulation of DNA damage in neurons.
Ku70 Binding (interacts) of mutant Htt in neurons
11) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.54 Pain Relevance 0
Mutant huntingtin impairs Ku70-mediated DNA repair

Mutant huntingtin prevents interaction of the DNA damage repair complex component Ku70 with damaged DNA, blocking repair of double-strand breaks.


Ku70 Binding (interaction) of huntingtin
12) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Title Doc Link PMC2867301 Disease Relevance 0.41 Pain Relevance 0
These data collectively suggest that the shorter Htt exon 1 peptides, including the polyQ tract, do interact with Ku70 and that mutant Htt interacts with Ku70 more strongly than wild-type Htt.
Ku70 Binding (interact) of Htt
13) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0.04
The early up-regulation of Ku70 and Ku80 probably occurs as a secondary response to DNA damage (Browne et al., 1999) induced by oxidative damage and by impaired DNA–PK activity as a result of an interaction between Ku70 and mutant Htt (Fig. 4 A).
Ku70 Binding (interaction) of mutant Htt
14) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.09 Pain Relevance 0
Furthermore, we titrated the amount of mutant Htt necessary for the interaction with Ku70 by using stable T-Rex–HeLa cells in which expression levels of mutant Htt can be controlled by the concentration of tetracyclin in the culture medium.
Ku70 Binding (interaction) of mutant Htt in HeLa
15) Confidence 0.25 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0
Interaction between mutant Htt and Ku70 impairs DNA repair function of the DNA–PK complex
Ku70 Binding (Interaction) of mutant Htt
16) Confidence 0.22 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0 Pain Relevance 0
Next, we confirmed the interaction between the mutant Htt exon 1 peptide and endogenous Ku70 by IP with R6/2 mouse brain (cerebral cortex and striatum) tissues (Fig. 3 A).
Ku70 Binding (interaction) of mutant Htt in striatum associated with cerebral cortex
17) Confidence 0.22 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.11 Pain Relevance 0.05
Next, we confirmed the interaction between the mutant Htt exon 1 peptide and endogenous Ku70 by IP with R6/2 mouse brain (cerebral cortex and striatum) tissues (Fig. 3 A).
Ku70 Binding (interaction) of mutant Htt in cerebral cortex associated with cerebral cortex
18) Confidence 0.08 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.11 Pain Relevance 0.05

General Comments

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