| pubmed-article:20298786 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20298786 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:20298786 | lifeskim:mentions | umls-concept:C0031760 | lld:lifeskim |
| pubmed-article:20298786 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:20298786 | lifeskim:mentions | umls-concept:C0039938 | lld:lifeskim |
| pubmed-article:20298786 | lifeskim:mentions | umls-concept:C0011164 | lld:lifeskim |
| pubmed-article:20298786 | lifeskim:mentions | umls-concept:C0815279 | lld:lifeskim |
| pubmed-article:20298786 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20298786 | pubmed:dateCreated | 2010-5-3 | lld:pubmed |
| pubmed-article:20298786 | pubmed:abstractText | The Tubby mouse is a phenotypic model for sensorineural deafness and retinal dystrophy including Usher syndrome type 1. Thioredoxin is a small 13kDa protein which, when ubiquitously expressed as a transgene in the mouse, provides protection against multiple disease states including light-induced and oxidative stress-induced neurodegeneration and is down-regulated in the Tubby retina. We tested if overexpression of human thioredoxin in the Tubby mouse inhibits retinal degeneration and loss of visual function. Electroretinography, immunocytochemistry, quantitative histology, RT-PCR and Western blots were used to obtain data which showed that thioredoxin overexpression prevented loss of photoreceptors and retinal function. Analysis of signal pathways showed that thioredoxin up-regulated neurotrophic factors BDNF and GDNF and activated survival signaling pathways Akt, Ras/Raf1/ and the ERKs while inhibiting the ASK1/JNK apoptosis pathway. Relationships between the Tubby gene, its pathological phenotype and regulation of the thioredoxin system remain to be established. | lld:pubmed |
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| pubmed-article:20298786 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20298786 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20298786 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20298786 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20298786 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20298786 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:20298786 | pubmed:issn | 1095-953X | lld:pubmed |
| pubmed-article:20298786 | pubmed:author | pubmed-author:KralRR | lld:pubmed |
| pubmed-article:20298786 | pubmed:author | pubmed-author:LiFengF | lld:pubmed |
| pubmed-article:20298786 | pubmed:author | pubmed-author:CaoWeiW | lld:pubmed |
| pubmed-article:20298786 | pubmed:author | pubmed-author:ZhouXiaohongX | lld:pubmed |
| pubmed-article:20298786 | pubmed:author | pubmed-author:YodoiJuniJ | lld:pubmed |
| pubmed-article:20298786 | pubmed:author | pubmed-author:McGinnisJames... | lld:pubmed |
| pubmed-article:20298786 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20298786 | pubmed:volume | 38 | lld:pubmed |
| pubmed-article:20298786 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20298786 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20298786 | pubmed:pagination | 446-55 | lld:pubmed |
| pubmed-article:20298786 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
