| pubmed-article:12560552 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12560552 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:12560552 | lifeskim:mentions | umls-concept:C0011164 | lld:lifeskim |
| pubmed-article:12560552 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:12560552 | pubmed:issue | 5607 | lld:pubmed |
| pubmed-article:12560552 | pubmed:dateCreated | 2003-1-31 | lld:pubmed |
| pubmed-article:12560552 | pubmed:abstractText | mahoganoid is a mouse coat-color mutation whose pigmentary phenotype and genetic interactions resemble those of Attractin (Atrn). Atrn mutations also cause spongiform neurodegeneration. Here, we show that a null mutation for mahoganoid causes a similar age-dependent neuropathology that includes many features of prion diseases but without accumulation of protease-resistant prion protein. The gene mutated in mahoganoid encodes a RING-containing protein with E3 ubiquitin ligase activity in vitro. Similarities in phenotype, expression, and genetic interactions suggest that mahoganoid and Atrn genes are part of a conserved pathway for regulated protein turnover whose function is essential for neuronal viability. | lld:pubmed |
| pubmed-article:12560552 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12560552 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12560552 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12560552 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12560552 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12560552 | pubmed:issn | 1095-9203 | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:WatsonStanley... | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:BarshGregory... | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:GunnTeresa... | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:JacksonPeter... | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:HeLinL | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:EldridgeAdam... | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:LuXin-YunXY | lld:pubmed |
| pubmed-article:12560552 | pubmed:author | pubmed-author:JollyAaron... | lld:pubmed |
| pubmed-article:12560552 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12560552 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:12560552 | pubmed:volume | 299 | lld:pubmed |
| pubmed-article:12560552 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12560552 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12560552 | pubmed:pagination | 710-2 | lld:pubmed |
| pubmed-article:12560552 | pubmed:dateRevised | 2007-3-19 | lld:pubmed |
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| pubmed-article:12560552 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12560552 | pubmed:articleTitle | Spongiform degeneration in mahoganoid mutant mice. | lld:pubmed |
| pubmed-article:12560552 | pubmed:affiliation | Department of Pediatrics, Department of Genetics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. | lld:pubmed |
| pubmed-article:12560552 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12560552 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12560552 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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