INT135045

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Context Info
Confidence 0.78
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 34
Total Number 38
Disease Relevance 11.59
Pain Relevance 0.36

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

peptidase activity (Atxn3) nucleus (Atxn3) cytoplasm (Atxn3)
Anatomy Link Frequency
brain 6
forebrain 1
nucleus 1
midbrain 1
Atxn3 (Mus musculus)
Atxn3 - C14A (1)
Pain Link Frequency Relevance Heat
midbrain 29 98.36 Very High Very High Very High
anesthesia 1 96.52 Very High Very High Very High
Pain 29 79.32 Quite High
Calcium channel 39 51.12 Quite High
imagery 34 24.72 Low Low
Central nervous system 29 5.00 Very Low Very Low Very Low
ketamine 29 5.00 Very Low Very Low Very Low
analgesia 10 5.00 Very Low Very Low Very Low
cerebral cortex 5 5.00 Very Low Very Low Very Low
Enkephalin 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ataxia 98 100.00 Very High Very High Very High
Machado-joseph Disease 364 99.36 Very High Very High Very High
Disease 831 99.34 Very High Very High Very High
Targeted Disruption 707 99.32 Very High Very High Very High
Toxicity 555 99.12 Very High Very High Very High
Neurodegenerative Disease 114 97.44 Very High Very High Very High
Cytomegalovirus Infection 29 96.56 Very High Very High Very High
Frontotemporal Dementia 8 94.32 High High
Parkinson's Disease 9 92.88 High High
Spinocerebellar Ataxia Type 2 38 91.04 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Recombinant 2UIM, 3UIM, and C14A ataxin-3(Q22) were expressed in BL21-A1 E. coli (Invitrogen Cat #C607003) as GST fusion proteins and purified as follows.
Gene_expression (expressed) of ataxin-3 (C14A)
1) Confidence 0.78 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0 Pain Relevance 0
Here we have demonstrated that alternative splicing of sequences distinct from the polyglutamine-encoding repeat can result in the production of an unstable, aggregate-prone ataxin-3 isoform, which results in increased insoluble aggregates in one murine model of SCA3.
Gene_expression (production) of ataxin-3 isoform associated with machado-joseph disease
2) Confidence 0.78 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.67 Pain Relevance 0
This mirrored the expression pattern of human ATXN3 variants in three sources: nonexpanded MJD15.4 transgenic mice (Figure 1C), CAG repeat-expanded MJD84.2 transgenic mice, and cDNA from pooled adult or fetal human brain tissue (Figure 1D).
Gene_expression (expression) of ATXN3 in brain associated with targeted disruption
3) Confidence 0.78 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.34 Pain Relevance 0
We transiently expressed these forms of ataxin-3 in Cos7 cells (Figure 4A and 4B) or HEK293T cells (data not shown) for 48 hours.
Gene_expression (expressed) of ataxin-3
4) Confidence 0.67 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.15 Pain Relevance 0
Although 2UIM and 3UIM ataxin-3 are both considered “full length” ataxin-3 isoforms, and both have been used in mechanistic studies of SCA3, the impact of this 3?
Gene_expression (isoforms) of ataxin-3 associated with machado-joseph disease
5) Confidence 0.67 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.65 Pain Relevance 0
Ataxin-3 adopts a unique conformation when expressed within the nucleus of transfected cells.
Gene_expression (expressed) of Ataxin-3 in nucleus
6) Confidence 0.60 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.30 Pain Relevance 0
To address the possibility that this increased aggregation of 2UIM ataxin-3 reflects transient overexpression in nonneuronal cells, we compared levels of SDS-insoluble ataxin-3 aggregates in whole brain lysates from aged MJD84.2 mice, which express primarily expanded Q84 3UIM ataxin-3 transprotein, and Q71B mice, which only express expanded Q71 2UIM ataxin-3 transprotein (Figure 4C and 4D).
Gene_expression (express) of ataxin-3 transprotein in brain
7) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.09 Pain Relevance 0
In more physiological 3UIM-predominant disease models, small increases in 2UIM ataxin-3 protein expression in restricted cell populations could serve as a fibrillization nidus, facilitating recruitment of expanded 3UIM ataxin-3 into toxic intranuclear microaggregates.
Gene_expression (expression) of ataxin-3 protein associated with disease
8) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.27 Pain Relevance 0
This could be physiologically significant in cells endogenously expressing small quantities of 2UIM ataxin-3 protein, as aggregate seeding is a kinetic barrier to misfolded protein fibrillization, and nucleoplasmic ataxin-3 misfolding is critical for disease pathogenesis.
Gene_expression (expressing) of ataxin-3 protein associated with disease
9) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.09 Pain Relevance 0
Given its longer repeat size, ataxin-3(Q84) in MJD84.2 mice might be expected to aggregate at least as readily as ataxin-3(Q71) expressed in Q71 B mice, provided that 2UIM and 3UIM ataxin-3 behave similarly in vivo.
Gene_expression (expressed) of ataxin-3
10) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.07 Pain Relevance 0
Cells expressing 2UIM ataxin-3 displayed moderately robust aggregation that was not observed in cells expressing 3UIM ataxin-3 or UIM3-mutant ataxin-3.
Gene_expression (expressing) of ataxin-3
11) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.11 Pain Relevance 0
To address the possibility that this increased aggregation of 2UIM ataxin-3 reflects transient overexpression in nonneuronal cells, we compared levels of SDS-insoluble ataxin-3 aggregates in whole brain lysates from aged MJD84.2 mice, which express primarily expanded Q84 3UIM ataxin-3 transprotein, and Q71B mice, which only express expanded Q71 2UIM ataxin-3 transprotein (Figure 4C and 4D).
Gene_expression (express) of ataxin-3 transprotein in brain
12) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.09 Pain Relevance 0
splice variants are expressed, 3UIM ataxin-3 is the predominant isoform.
Gene_expression (expressed) of 3UIM ataxin-3
13) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.62 Pain Relevance 0
In some circumstances, such as defined in vitro systems exploring ataxin-3 DUB activity, 2UIM ataxin-3 and 3UIM ataxin-3 behave nearly identically and will produce similar results.
Gene_expression (behave) of 3UIM ataxin-3
14) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.69 Pain Relevance 0
In cells, transient transfections of equivalent amounts of 2UIM and 3UIM ataxin-3 expression vectors consistently yielded lower amounts of 2UIM protein.
Gene_expression (expression) of 3UIM ataxin-3
15) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0 Pain Relevance 0
Although 2UIM and 3UIM ataxin-3 are both considered “full length” ataxin-3 isoforms, and both have been used in mechanistic studies of SCA3, the impact of this 3?
Gene_expression (considered) of 3UIM ataxin-3 associated with machado-joseph disease
16) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.66 Pain Relevance 0.03
We further show that although C-terminal splice isoform variation does not influence ataxin-3?
Neg (not) Gene_expression (influence) of ataxin-3
17) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.48 Pain Relevance 0
In some circumstances, such as defined in vitro systems exploring ataxin-3 DUB activity, 2UIM ataxin-3 and 3UIM ataxin-3 behave nearly identically and will produce similar results.
Gene_expression (behave) of 2UIM ataxin-3
18) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.70 Pain Relevance 0
In some circumstances, such as defined in vitro systems exploring ataxin-3 DUB activity, 2UIM ataxin-3 and 3UIM ataxin-3 behave nearly identically and will produce similar results.
Gene_expression (produce) of 2UIM ataxin-3
19) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.71 Pain Relevance 0
Briefly, Q28 ataxin-3 was amplified using MJD.Nter.F#722 (see below) and the primer hMJD2UIM-R1N (5?
Gene_expression (amplified) of ataxin-3
20) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965175 Disease Relevance 0.27 Pain Relevance 0.08

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