INT181802

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.65
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 3.15
Pain Relevance 0

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
neurons 1
gland 1
Atxn1 (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 1 33.84 Quite Low
Calcium channel 16 5.00 Very Low Very Low Very Low
Action potential 7 5.00 Very Low Very Low Very Low
anesthesia 4 5.00 Very Low Very Low Very Low
Migraine 3 5.00 Very Low Very Low Very Low
Kinase C 3 5.00 Very Low Very Low Very Low
isoflurane 3 5.00 Very Low Very Low Very Low
Thoracotomy 2 5.00 Very Low Very Low Very Low
Potency 2 5.00 Very Low Very Low Very Low
fibrosis 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 85 99.80 Very High Very High Very High
Myocardial Infarction 84 98.84 Very High Very High Very High
Ataxia 99 98.80 Very High Very High Very High
Targeted Disruption 31 98.20 Very High Very High Very High
Salivary Gland Disease 12 89.64 High High
Spinocerebellar Ataxia Type 2 51 77.16 Quite High
Dilated Cardiomyopathy 1 71.32 Quite High
Aging 1 47.12 Quite Low
Infarction 7 44.60 Quite Low
Hypertrophy 1 41.28 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Although nuclear localization of ataxin-1 is necessary for the development of the disease, nuclear aggregation of ataxin-1 is not required to initiate pathogenesis in transgenic mice (Klement et al 1998).
Localization (localization) of ataxin-1 associated with targeted disruption and disease
1) Confidence 0.65 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.77 Pain Relevance 0
Although nuclear localization of ataxin-1 is necessary for the development of the disease, nuclear aggregation of ataxin-1 is not required to initiate pathogenesis in transgenic mice (Klement et al 1998).
Localization (aggregation) of ataxin-1 associated with targeted disruption and disease
2) Confidence 0.61 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.78 Pain Relevance 0
Cummings et al (1998) found colocalization of the 20S proteosome and chaperone HSJ2, a member of the Hsp40 family, with large nuclear inclusions of ataxin-1 in brain neurons of patients with SCA1 and in mice transgenic for a mutant SCA1 allele containing 82 glutamines.
Localization (colocalization) of ataxin-1 in neurons associated with targeted disruption
3) Confidence 0.61 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.73 Pain Relevance 0
Along these lines, fractionation of Spoc cells based on Sca-1 greatly enriches for a population of cells in the Sca-1?
Localization (based) of Sca-1
4) Confidence 0.38 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1064849 Disease Relevance 0.37 Pain Relevance 0
Sca-1 localization was confirmed to be expressed on duct cells on the periphery of cultured Sca-1 (Ly-6A) gland-derived spheres (Fig.
Localization (localization) of Sca-1 in gland
5) Confidence 0.33 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2329592 Disease Relevance 0.18 Pain Relevance 0
Immuno labeling on different sections after MI confirmed the flow cytometric analysis, demonstrating co-localization of LacZ+ nuclei with Sca-1, CD31, and CD45 (Fig. 4b–d).
Localization (localization) of Sca-1 associated with myocardial infarction
6) Confidence 0.09 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916122 Disease Relevance 0.32 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox