INT181803

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Context Info
Confidence 0.48
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 7.00
Pain Relevance 0.30

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

nucleoplasm (Atxn1) RNA binding (Atxn1) nucleus (Atxn1)
cytoplasm (Atxn1)
Anatomy Link Frequency
cardiomyocytes 2
Purkinje cells 1
Atxn1 (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 29 84.72 Quite High
depression 4 84.16 Quite High
amygdala 24 67.80 Quite High
anesthesia 8 61.84 Quite High
Calcium channel 18 51.00 Quite High
Hippocampus 25 42.32 Quite Low
Pyramidal cell 28 34.40 Quite Low
agonist 3 28.44 Quite Low
Action potential 21 5.00 Very Low Very Low Very Low
cerebral cortex 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Spinocerebellar Ataxia Type 2 204 100.00 Very High Very High Very High
Disease 227 99.90 Very High Very High Very High
Myocardial Infarction 45 99.12 Very High Very High Very High
Targeted Disruption 116 98.36 Very High Very High Very High
Repression 5 98.32 Very High Very High Very High
Aging 6 96.24 Very High Very High Very High
Anxiety Disorder 83 94.00 High High
Cognitive Disorder 29 93.32 High High
Neurodegenerative Disease 31 91.36 High High
Ataxia 110 89.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Caused by an expanded polyglutamine tract in ataxin 1 (ATXN1), SCA1 pathogenesis involves a multifactorial process that likely begins with misfolding of ATXN1, which has functional consequences on its interactions, leading to transcriptional dysregulation.
ATXN1 Binding (interactions) of associated with spinocerebellar ataxia type 2
1) Confidence 0.48 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1880853 Disease Relevance 0.77 Pain Relevance 0
Although ataxin-1 and ataxin-2 interact physically and genetically [37.38], the knockout phenotypes of the respective genes show little overlap [16] with the caveat that innate and learned fear behaviors were not reported for Atxn1 ko mice.


ataxin-1 Binding (interact) of associated with targeted disruption and anxiety disorder
2) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2707006 Disease Relevance 1.10 Pain Relevance 0.17
LANP is expressed predominantly in Purkinje cells, and its interaction with ataxin-1 is significantly stronger when the number of glutamines is increased (Matilla et al 1997).
ataxin-1 Binding (interaction) of in Purkinje cells
3) Confidence 0.39 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.74 Pain Relevance 0
Overexpression of HSJ2 in these cells reduces aggregation of ataxin-1, suggesting a possible therapeutic strategy.
ataxin-1 Binding (aggregation) of
4) Confidence 0.39 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.41 Pain Relevance 0
Caused by an expanded polyglutamine tract in ataxin 1 (ATXN1), SCA1 pathogenesis involves a multifactorial process that likely begins with misfolding of ATXN1, which has functional consequences on its interactions, leading to transcriptional dysregulation.
ATXN1 Binding (leading) of associated with spinocerebellar ataxia type 2
5) Confidence 0.37 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1880853 Disease Relevance 0.78 Pain Relevance 0
These mice develop symptoms similar to those seen in people with SCA1.
SCA1 Binding (people) of associated with spinocerebellar ataxia type 2
6) Confidence 0.37 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1880853 Disease Relevance 0.97 Pain Relevance 0.04
Ataxin-1 binds chromosomes and mediates transcriptional repression when tethered to DNA.
Ataxin-1 Binding (binds) of associated with repression
7) Confidence 0.29 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.21 Pain Relevance 0
fraction, the former cells rapidly adhere to the plate and, with the exception of a few putative contaminating Sca-1?
Sca-1 Neg (exception) Binding (adhere) of
8) Confidence 0.19 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1064849 Disease Relevance 0 Pain Relevance 0.03
This is consistent with the increased magnitude and kinetics of cardiomyocyte differentiation observed when the Sca-1?
Sca-1 Binding (observed) of in cardiomyocyte
9) Confidence 0.19 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1064849 Disease Relevance 0.32 Pain Relevance 0
fraction that in vitro become beating cardiomyocytes; however, engraftment of these Sca-1?
Sca-1 Binding (engraftment) of in cardiomyocytes
10) Confidence 0.19 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1064849 Disease Relevance 0.36 Pain Relevance 0
Our group showed that two polyQ disease proteins (HD and SCA1) interact and reduce high mobility group protein B proteins (Qi et al., 2007) essential for the repair of DNA double-strand breaks (DSBs) occurring naturally in transcription (Travers, 2003; Bianchi and Agresti, 2005; Ju et al., 2006).
SCA1 Binding (interact) of associated with disease
11) Confidence 0.18 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 1.05 Pain Relevance 0
The cells were then trypsinized for 1 minute, centrifuged, washed with PBS, fixed in 4% paraformaldehyde for 0.5 hour at room temperature, washed and blocked in 2%FCS for 0.5 hour at room temperature with agitation. 1.5×105cells were then incubated with each of the following conjugated monoclonal antibodies: Tie-2, Flk-1, CD34, c-Kit, Thy-1, Sca-1 (PharMingen, San Diego, CA) for 90 mins at room temperature.
Sca-1 Binding (temperature) of
12) Confidence 0.14 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762397 Disease Relevance 0.30 Pain Relevance 0.06

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