| pubmed-article:17189700 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C1522424 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0035309 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0752125 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:17189700 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:17189700 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:17189700 | pubmed:dateCreated | 2007-3-2 | lld:pubmed |
| pubmed-article:17189700 | pubmed:abstractText | We have approached the role of cellular stress in neurodegenerative diseases caused by polyglutamine expansion (polyQ) in the context of Spinocerebellar ataxia type 7 (SCA7) that includes retinal degeneration. Using the R7E mouse, in which polyQ-ataxin-7 is specifically over-expressed in rod photoreceptors, we previously showed that rod dysfunction correlated to moderate and prolonged activation of the JNK/c-Jun stress pathway. SCA7 retinopathy was also associated with reduced expression of rod-specific genes, including the transcription factor Nrl, which is essential for rod differentiation and function. Here, we report that R7E retinopathy is improved upon breeding with the JunAA knock-in mice, in which JNK-mediated activation of c-Jun is compromised. Expression of Nrl and its downstream targets, which are involved in phototranduction, are partially restored in the JunAA-R7E mice. We further show that c-Jun can directly repress the transcription of Nrl. Our studies suggest that polyQ-induced cellular stress leads to repression of genes necessary for neuronal fate and function. | lld:pubmed |
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| pubmed-article:17189700 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17189700 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17189700 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17189700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17189700 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17189700 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:17189700 | pubmed:issn | 0969-9961 | lld:pubmed |
| pubmed-article:17189700 | pubmed:author | pubmed-author:SwaroopAnandA | lld:pubmed |
