INT181809

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Context Info
Confidence 0.77
First Reported 2005
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 81
Total Number 82
Disease Relevance 28.66
Pain Relevance 1.42

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
stem cell 7
bone marrow 3
hematopoietic stem cells 3
neurons 3
stem 2
Atxn1 (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 10 91.88 High High
cytokine 24 91.64 High High
Inflammation 72 91.60 High High
Glutamate 20 89.48 High High
ischemia 22 86.76 High High
excitatory amino acid 10 83.56 Quite High
anesthesia 74 77.00 Quite High
cerebral cortex 18 75.20 Quite High
depression 10 75.20 Quite High
Kinase C 13 74.56 Quite High
Disease Link Frequency Relevance Heat
Spinocerebellar Ataxia Type 2 522 100.00 Very High Very High Very High
Disease 495 100.00 Very High Very High Very High
Ataxia 130 100.00 Very High Very High Very High
Death 73 99.80 Very High Very High Very High
Infection 178 99.74 Very High Very High Very High
Targeted Disruption 386 99.72 Very High Very High Very High
Cancer 1573 99.38 Very High Very High Very High
Myocardial Infarction 944 98.60 Very High Very High Very High
Carcinoma 119 98.28 Very High Very High Very High
Neurodegenerative Disease 113 96.60 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our trials in a faithful mouse model of SCA1, which expresses endogenous levels of mutant, full-length ATXN1 protein in a proper spatial and temporal pattern and reproduces many features of the human disease, strongly suggest that the therapeutic potential of lithium in this disease deserves serious consideration.
Gene_expression (expresses) of SCA1 associated with spinocerebellar ataxia type 2 and disease
1) Confidence 0.77 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 1.02 Pain Relevance 0.17
Our trials in a faithful mouse model of SCA1, which expresses endogenous levels of mutant, full-length ATXN1 protein in a proper spatial and temporal pattern and reproduces many features of the human disease, strongly suggest that the therapeutic potential of lithium in this disease deserves serious consideration.
Gene_expression (expresses) of ATXN1 associated with spinocerebellar ataxia type 2 and disease
2) Confidence 0.77 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 1.03 Pain Relevance 0.17
In SCA1, the abnormal protein is ataxin 1, which is made in many neurons including the cerebellar neurons (Purkinje cells) that coordinate movement.


Gene_expression (made) of ataxin 1 in neurons associated with spinocerebellar ataxia type 2
3) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1880853 Disease Relevance 1.62 Pain Relevance 0
Therefore, we rationalized that if we use a drug that enhances gene expression, we might slow SCA1 progression.
Gene_expression (progression) of SCA1 associated with spinocerebellar ataxia type 2
4) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 0.71 Pain Relevance 0.11
Here, we show the beneficial effects of chronic lithium treatment on multiple measures in an SCA1 disease model—Sca1154Q/2Q mice—that express the full-length mutant protein in the endogenous spatiotemporal pattern and reproduce most features of human SCA1.
Gene_expression (features) of SCA1 associated with spinocerebellar ataxia type 2 and disease
5) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 0.75 Pain Relevance 0.03
Could the progression of SCA1 be slowed, therefore, by using an agent that affects gene expression?
Gene_expression (progression) of SCA1 associated with spinocerebellar ataxia type 2
6) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1880853 Disease Relevance 1.46 Pain Relevance 0.04
Our trials in a faithful mouse model of SCA1, which expresses endogenous levels of mutant, full-length ATXN1 protein in a proper spatial and temporal pattern and reproduces many features of the human disease, strongly suggest that the therapeutic potential of lithium in this disease deserves serious consideration.
Gene_expression (expresses) of SCA1 associated with spinocerebellar ataxia type 2 and disease
7) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 1.02 Pain Relevance 0.17
In SCA1, the abnormal protein is ataxin 1, which is made in many neurons including the cerebellar neurons (Purkinje cells) that coordinate movement.


Gene_expression (made) of SCA1 in neurons associated with spinocerebellar ataxia type 2
8) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1880853 Disease Relevance 1.64 Pain Relevance 0
Similar colocalization can be seen in HeLa cells transfected with ataxin-1.
Gene_expression (transfected) of ataxin-1 in HeLa
9) Confidence 0.63 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.56 Pain Relevance 0
Here, we show the beneficial effects of chronic lithium treatment on multiple measures in an SCA1 disease model—Sca1154Q/2Q mice—that express the full-length mutant protein in the endogenous spatiotemporal pattern and reproduce most features of human SCA1.
Gene_expression (express) of SCA1 associated with spinocerebellar ataxia type 2 and disease
10) Confidence 0.60 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 0.85 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.
Gene_expression (allele) of SCA1 in neurons associated with targeted disruption
11) Confidence 0.55 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 0.62 Pain Relevance 0
The Sca1154Q/2Q knock-in mouse model bears 154 CAG repeats in the mouse Sca1 locus and expresses full-length mutant ATXN1 in its endogenous expression pattern and context [18].
Gene_expression (expresses) of ATXN1 associated with targeted disruption
12) Confidence 0.52 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 0.97 Pain Relevance 0.12
The source of the mutation in many genetic subtypes of ataxias (SCA1, SCA2, SCA3, SCA6, SCA7, SCA12, and SCA17) is the same (CAG repeat expansion), and the resulting protein product contains a long polyglutamine domain.
Gene_expression (source) of SCA1 associated with ataxia
13) Confidence 0.49 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413192 Disease Relevance 1.10 Pain Relevance 0
In low-grade WAP-T tumors we noted that Thy1 as well as Sca1 expression is mostly restricted to the stromal compartment and to adjacent tumor cells (Figure 8E).
Gene_expression (expression) of Sca1 associated with cancer
14) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2920333 Disease Relevance 0.58 Pain Relevance 0
While the RNA levels of the Cd24a and Cd49f genes positively correlated with increased cell density, expression of the Sca1 decreased as a function of cell density (Figure 10C).
Gene_expression (expression) of Sca1
15) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2920333 Disease Relevance 0 Pain Relevance 0
In high-grade carcinomas a subset of cells adjacent to the stroma, demarked by the strong expression of Thy1, expresses either Thy1 or Sca1 or both markers (Figure 8F).
Gene_expression (expresses) of Sca1 in stroma associated with carcinoma
16) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2920333 Disease Relevance 0.62 Pain Relevance 0
Cellular subsets sorted according to expression of CD24a, CD49f, CD61, Epcam, Sca1, and Thy1 cell surface proteins, or metabolic markers (e.g.
Gene_expression (expression) of Sca1
17) Confidence 0.42 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2920333 Disease Relevance 0.64 Pain Relevance 0
To substantiate this idea, 5×103 and 5×104 FACS-sorted CD24alow/CD49flow G-2 cells were plated per well, and after 5 days in culture expression of the Cd24a, Cd49f and Sca1 genes was quantified by qPCR.
Gene_expression (expression) of Sca1
18) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2920333 Disease Relevance 0 Pain Relevance 0
Therefore, we aimed to characterize the differences between stem and progenitor cells in vitro by analyzing the differentiation capacities of these cells using three approaches: biochemical assays, morphological characterization and genetic analysis involving Opn, CatK and Sca-1 expressions.
Gene_expression (expressions) of Sca-1 in stem
19) Confidence 0.38 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2984396 Disease Relevance 0.22 Pain Relevance 0
The onset of differentiation after 5 days of culture and the gradual loss of Sca-1, c-Kit and Musashi-1 expression after 3 days of culture indicated that for subsequent functional experiments employing transplantation, cells that had been cultured for 3 days were most suitable.


Gene_expression (expression) of Sca-1
20) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2329592 Disease Relevance 0 Pain Relevance 0

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