| pubmed-article:19165829 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19165829 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:19165829 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:19165829 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:19165829 | lifeskim:mentions | umls-concept:C1420308 | lld:lifeskim |
| pubmed-article:19165829 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:19165829 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19165829 | pubmed:dateCreated | 2009-3-30 | lld:pubmed |
| pubmed-article:19165829 | pubmed:abstractText | The extracellular isoform of superoxide dismutase (EC-SOD, Sod3) plays a protective role against various diseases and injuries mediated by oxidative stress. To investigate the pathophysiological roles of EC-SOD, we generated tetracycline-inducible Sod3 transgenic mice and directed the tissue-specific expression of transgenes by crossing Sod3 transgenic mice with tissue-specific transactivator transgenics. Double transgenic mice with liver-specific expression of Sod3 showed increased EC-SOD levels predominantly in the plasma as the circulating form, whereas double transgenic mice with neuronal-specific expression expressed higher levels of EC-SOD in hippocampus and cortex with intact EC-SOD as the dominant form. EC-SOD protein levels also correlated well with increased SOD activities in double transgenic mice. In addition to enabling tissue-specific expression, the transgene expression can be quickly turned on and off by doxycycline supplementation in the mouse chow. This mouse model, thus, provides the flexibility for on-off control of transgene expression in multiple target tissues. | lld:pubmed |
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| pubmed-article:19165829 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19165829 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19165829 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19165829 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19165829 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:19165829 | pubmed:issn | 1526-968X | lld:pubmed |
| pubmed-article:19165829 | pubmed:author | pubmed-author:HuangTing-Tin... | lld:pubmed |
| pubmed-article:19165829 | pubmed:author | pubmed-author:FikeJohn RJR | lld:pubmed |
| pubmed-article:19165829 | pubmed:author | pubmed-author:ZouYaniY | lld:pubmed |
| pubmed-article:19165829 | pubmed:author | pubmed-author:ChenChih-Hsin... | lld:pubmed |
| pubmed-article:19165829 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19165829 | pubmed:volume | 47 | lld:pubmed |
| pubmed-article:19165829 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19165829 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19165829 | pubmed:pagination | 142-54 | lld:pubmed |
| pubmed-article:19165829 | pubmed:dateRevised | 2011-7-20 | lld:pubmed |
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| pubmed-article:19165829 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19165829 | pubmed:articleTitle | A new mouse model for temporal- and tissue-specific control of extracellular superoxide dismutase. | lld:pubmed |
| pubmed-article:19165829 | pubmed:affiliation | Department of Neurology and Neurological Sciences, Stanford University, Stanford, California, USA. | lld:pubmed |
| pubmed-article:19165829 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19165829 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:19165829 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19165829 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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