| pubmed-article:9353349 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1335872 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1335873 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1513095 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1179435 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1416479 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1705248 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1548799 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C1524073 | lld:lifeskim |
| pubmed-article:9353349 | lifeskim:mentions | umls-concept:C0449432 | lld:lifeskim |
| pubmed-article:9353349 | pubmed:issue | 45 | lld:pubmed |
| pubmed-article:9353349 | pubmed:dateCreated | 1997-12-12 | lld:pubmed |
| pubmed-article:9353349 | pubmed:abstractText | The mechanism of IFN resistance was examined in three long-term cell lines, SK-MEL-28, SK-MEL-3, and MM96, exhibiting significant variation in responsiveness to the antiproliferative and antiviral effects of type I IFNs. The JAK-STAT components involved in IFN signal transduction were analyzed in detail. After exposure to IFN, activation of the IFN type I receptor-linked tyrosine kinases, JAK-1 and TYK-2, was detected at similar levels in both IFN-sensitive and IFN-resistant cell types, indicating that IFN resistance did not result from a deficiency in signaling at the level of receptor-associated kinase activation. However, analysis of ISGF3 transcription factor components, STAT1, STAT2, and p48-ISGF3gamma, revealed that their expression and activation correlated with cellular IFN responsiveness. The analysis was extended to also include IFN-sensitive primary melanocytes, three additional IFN-resistant melanoma cell lines, and seven cell cultures recently established from melanoma patient biopsies. It was consistently observed that the most marked difference in ISGF3 was a lack of STAT1 in the resistant versus the sensitive cells. Transfection of the IFN-resistant MM96 cell line to express increased levels of STAT1 protein partially restored IFN responsiveness in an antiviral assay. We conclude that a defect in the level of STAT1 and possibly all three ISGF3 components in IFN-resistant human melanoma cells may be a general phenomenon responsible for reduced cellular responsiveness of melanomas to IFNs. | lld:pubmed |
| pubmed-article:9353349 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9353349 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9353349 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9353349 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:9353349 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:HerseyPP | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:TamN DND | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:DevenishR JRJ | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:EdmondsonSS | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:KrauerK GKG | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:RalphS JSJ | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:Hatzinisiriou... | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:WongL HLH | lld:pubmed |
| pubmed-article:9353349 | pubmed:author | pubmed-author:EstcourtM JMJ | lld:pubmed |
| pubmed-article:9353349 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9353349 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:9353349 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9353349 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9353349 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9353349 | pubmed:pagination | 28779-85 | lld:pubmed |
| pubmed-article:9353349 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:9353349 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9353349 | pubmed:articleTitle | Interferon-resistant human melanoma cells are deficient in ISGF3 components, STAT1, STAT2, and p48-ISGF3gamma. | lld:pubmed |
| pubmed-article:9353349 | pubmed:affiliation | Department of Biochemistry and Molecular Biology, Monash University, Wellington Road, Clayton, Victoria 3168, Australia. | lld:pubmed |
| pubmed-article:9353349 | pubmed:publicationType | Journal Article | lld:pubmed |
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