pubmed-article:18021406 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C1522424 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C0268281 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C1155266 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C0206256 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C0752248 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:18021406 | lifeskim:mentions | umls-concept:C1363844 | lld:lifeskim |
pubmed-article:18021406 | pubmed:dateCreated | 2008-1-17 | lld:pubmed |
pubmed-article:18021406 | pubmed:abstractText | The infantile form of neuronal ceroid lipofuscinosis (also known as infantile Batten disease) is caused by hereditary deficiency of a lysosomal enzyme, palmitoyl-protein thioesterase-1 (PPT1), and is characterized by severe cortical degeneration with blindness and cognitive and motor dysfunction. The PPT1-deficient knockout mouse recapitulates the key features of the disorder, including seizures and death by 7-9 months of age. In the current study, we compared gene expression profiles of whole brain from PPT1 knockout and normal mice at 3, 5 and 8 months of age to identify temporal changes in molecular pathways implicated in disease pathogenesis. | lld:pubmed |
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pubmed-article:18021406 | pubmed:language | eng | lld:pubmed |
pubmed-article:18021406 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18021406 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18021406 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18021406 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18021406 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18021406 | pubmed:issn | 1471-2202 | lld:pubmed |
pubmed-article:18021406 | pubmed:author | pubmed-author:LuJui-YunJY | lld:pubmed |
pubmed-article:18021406 | pubmed:author | pubmed-author:HofmannSandra... | lld:pubmed |
pubmed-article:18021406 | pubmed:author | pubmed-author:QiaoXingwenX | lld:pubmed |
pubmed-article:18021406 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18021406 | pubmed:volume | 8 | lld:pubmed |
pubmed-article:18021406 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18021406 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18021406 | pubmed:pagination | 95 | lld:pubmed |
pubmed-article:18021406 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:18021406 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:18021406 | pubmed:articleTitle | Gene expression profiling in a mouse model of infantile neuronal ceroid lipofuscinosis reveals upregulation of immediate early genes and mediators of the inflammatory response. | lld:pubmed |
pubmed-article:18021406 | pubmed:affiliation | Hamon Center for Therapeutic Oncology Research and the Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. xingwen.qiao@utsouthwestern.edu | lld:pubmed |
pubmed-article:18021406 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18021406 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:18021406 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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