rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
50
|
pubmed:dateCreated |
2008-12-8
|
pubmed:abstractText |
Dermatomyositis (DM) is an autoimmune disease, which is often accompanied by the development of disease-specific autoantibodies directed against the SNF2-superfamily helicase, Mi-2. Recent evidence suggests that ultraviolet radiation exposure may be an important risk factor for the development of not only the disease but also specific autoimmunity against Mi-2. Consequently, we investigated the effects of ultraviolet radiation on Mi-2 protein expression. We observed an increase in protein levels upon ultraviolet radiation exposure in cell culture systems. These changes in expression occur quite rapidly, are maximized just 1 h following exposure, and are unique to Mi-2 when compared with other members of the NuRD complex. Changes in protein levels are not mediated through transcriptional mechanisms. Treatment results in a more efficiently translated message through regulatory elements in the 5'-UTR region of the transcript. Investigation into protein half-life further demonstrated increased stability of Mi-2 following UV exposure. Taken together, we describe a system by which Mi-2 protein expression can be quickly increased following UV exposure and then maintained up to 16 h later. These data provide a novel regulation of an important transcriptional regulator and provide insight into the possible mechanisms of the development of DM and associated autoantibodies.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-10204490,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-10626795,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-10748103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-10922072,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-12198550,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-12504018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-12509610,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-12821781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-12905483,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-15020040,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-15189737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-15358836,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-15728237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-15760588,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-15966133,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-16213212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-16932743,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-16966018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-17053509,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-17110150,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-17344210,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-17626165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-17694084,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-17761946,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-18319710,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-2409985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-8192178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-9663395,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-9790534,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-9804427,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18922793-9885572
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0021-9258
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
12
|
pubmed:volume |
283
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
34976-82
|
pubmed:dateRevised |
2010-9-21
|
pubmed:meshHeading |
pubmed-meshheading:18922793-5' Untranslated Regions,
pubmed-meshheading:18922793-Autoantibodies,
pubmed-meshheading:18922793-Autoantigens,
pubmed-meshheading:18922793-Cell Line, Tumor,
pubmed-meshheading:18922793-Cell Separation,
pubmed-meshheading:18922793-DNA Helicases,
pubmed-meshheading:18922793-Flow Cytometry,
pubmed-meshheading:18922793-Humans,
pubmed-meshheading:18922793-Keratinocytes,
pubmed-meshheading:18922793-Mi-2 Nucleosome Remodeling and Deacetylase Complex,
pubmed-meshheading:18922793-Models, Biological,
pubmed-meshheading:18922793-Plasmids,
pubmed-meshheading:18922793-Protein Biosynthesis,
pubmed-meshheading:18922793-Risk Factors,
pubmed-meshheading:18922793-Time Factors,
pubmed-meshheading:18922793-Transcription, Genetic,
pubmed-meshheading:18922793-Ultraviolet Rays
|
pubmed:year |
2008
|
pubmed:articleTitle |
UV radiation regulates Mi-2 through protein translation and stability.
|
pubmed:affiliation |
Laboratory of Molecular Carcinogenesis, NIEHS, National Intitutes of Health, Research Triangle Park, NC 27709, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Intramural
|