| pubmed-article:11580893 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C1522424 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C0035334 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C0752125 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C1413723 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C0665827 | lld:lifeskim |
| pubmed-article:11580893 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:11580893 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:11580893 | pubmed:dateCreated | 2001-10-2 | lld:pubmed |
| pubmed-article:11580893 | pubmed:abstractText | Spinocerebellar ataxia type 7 (SCA7) is an autosomal dominant disorder caused by a CAG repeat expansion. To determine the mechanism of neurotoxicity, we produced transgenic mice and observed a cone-rod dystrophy. Nuclear inclusions were present, suggesting that the disease pathway involves the nucleus. When yeast two-hybrid assays indicated that cone-rod homeobox protein (CRX) interacts with ataxin-7, we performed further studies to assess this interaction. We found that ataxin-7 and CRX colocalize and coimmunoprecipitate. We observed that polyglutamine-expanded ataxin-7 can dramatically suppress CRX transactivation. In SCA7 transgenic mice, electrophoretic mobility shift assays indicated reduced CRX binding activity, while RT-PCR analysis detected reductions in CRX-regulated genes. Our results suggest that CRX transcription interference accounts for the retinal degeneration in SCA7 and thus may provide an explanation for how cell-type specificity is achieved in this polyglutamine repeat disease. | lld:pubmed |
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| pubmed-article:11580893 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11580893 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11580893 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11580893 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:11580893 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:ChenSS | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:HurleyJ BJB | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:SmithA CAC | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:HuangJJ | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:WareC BCB | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:WangXX | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:LiL YLY | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:La SpadaA RAR | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:PtácekL JLJ | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:FuY HYH | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:MartinezR ARA | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:KoszdinK LKL | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:SopherB LBL | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:PossinD EDE | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:LibbyR TRT | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:TreutingP MPM | lld:pubmed |
| pubmed-article:11580893 | pubmed:author | pubmed-author:EinumD DDD | lld:pubmed |
| pubmed-article:11580893 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11580893 | pubmed:day | 27 | lld:pubmed |
| pubmed-article:11580893 | pubmed:volume | 31 | lld:pubmed |
| pubmed-article:11580893 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11580893 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11580893 | pubmed:pagination | 913-27 | lld:pubmed |
| pubmed-article:11580893 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11580893 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11580893 | pubmed:articleTitle | Polyglutamine-expanded ataxin-7 antagonizes CRX function and induces cone-rod dystrophy in a mouse model of SCA7. | lld:pubmed |
| pubmed-article:11580893 | pubmed:affiliation | Department of Laboratory Medicine, University of Washington Medical Center, Seattle, WA 98195, USA. laspada@u.washington.edu | lld:pubmed |
| pubmed-article:11580893 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11580893 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11580893 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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