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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1994-4-21
|
| pubmed:abstractText |
Tumorigenesis in mice of the rat insulin promoter [RIP]-simian virus 40 tumor antigen [SV40 Tag] transgenic lineages, RIP1-Tag2 and RIP1-Tag4, is a process initiated by expression of SV40 Tag in pancreatic beta cells, evolution of islet cell hyperplasia and insulinoma appearance. Analysis of major histocompatibility complex [MHC] class I gene expression during this process revealed a normal level of MHC class I molecules at the surface of pancreatic islet cells of RIP1-Tag4 mice, while hyperplastic islets from the same mice contained cells expressing a normal level and cells expressing a low level of MHC class I antigen. Insulinomas themselves expressed very low levels or no MHC class I gene product. Thus, down-regulation of MHC class I gene appears to accompany tumor progression of SV40 Tag-transformed beta islet cells. MHC class I antigen expression in a series of clonally derived cell lines of beta cell origin from different SV40 Tag-induced insulinomas ranged from quite low to undetectable, although expression was inducible by interferon-gamma. Nuclear run-on and transient transfection analyses indicated that expression of the MHC class I gene in these cells in controlled at the transcriptional level, and that the decreased expression is paralleled by reduced binding of transcription factors to the R1 element of the H-2 enhancer.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chloramphenicol O-Acetyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0950-9232
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
9
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1195-204
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:8134122-Animals,
pubmed-meshheading:8134122-Base Sequence,
pubmed-meshheading:8134122-Blotting, Northern,
pubmed-meshheading:8134122-Cell Line,
pubmed-meshheading:8134122-Cell Line, Transformed,
pubmed-meshheading:8134122-Chloramphenicol O-Acetyltransferase,
pubmed-meshheading:8134122-Down-Regulation,
pubmed-meshheading:8134122-Enhancer Elements, Genetic,
pubmed-meshheading:8134122-H-2 Antigens,
pubmed-meshheading:8134122-Histocompatibility Antigens Class I,
pubmed-meshheading:8134122-Insulinoma,
pubmed-meshheading:8134122-Interferon-gamma,
pubmed-meshheading:8134122-Islets of Langerhans,
pubmed-meshheading:8134122-Mice,
pubmed-meshheading:8134122-Mice, Inbred C57BL,
pubmed-meshheading:8134122-Molecular Sequence Data,
pubmed-meshheading:8134122-Transfection,
pubmed-meshheading:8134122-Tumor Cells, Cultured
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Down-regulation of MHC class I antigen in insulinoma cells controlled by the R1 element of the H-2 enhancer.
|
| pubmed:affiliation |
Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|