pubmed-article:15009724 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15009724 | lifeskim:mentions | umls-concept:C1513095 | lld:lifeskim |
pubmed-article:15009724 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:15009724 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:15009724 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:15009724 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:15009724 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:15009724 | pubmed:dateCreated | 2004-3-10 | lld:pubmed |
pubmed-article:15009724 | pubmed:abstractText | Interferon-gamma, a known inhibitor of tumor cell growth, has been used in several protocols for the treatment of melanoma. We have studied the molecular events underlying interferon-gamma-induced G0/G1 arrest in four metastatic melanoma cell lines with different responsiveness to interferon-gamma. The growth arrest did not result from enhanced expression of cyclin-dependent kinase inhibitors p21 and p27. Instead, it correlated with downregulation of cyclin E and cyclin A and inhibition of their associated kinase activities. We show that interferon-gamma-induced growth inhibition could be abrogated by overexpression of dominant negative STAT1 (signal transducer and activator of transcription 1) in the melanoma cell line A375, suggesting that STAT1 plays a crucial part for the anti-proliferative effect. Erythropoietin stimulation of a chimeric receptor led to a concentration-dependent STAT1 activation and concomitant growth arrest when it contained the STAT recruitment motif Y440 of the interferon-gamma receptor 1. In contrast, dose-response studies for interferon-gamma revealed a discrepancy between levels of STAT1 activation and the extent of growth inhibition; whereas STAT1 was activated by low doses of interferon-gamma (10 U per mL), growth inhibitory effects were only visible with 100-fold higher concentrations. Our results suggest the presence of additional signals emanating from the interferon-gamma receptor, which may counteract the anti-proliferative function of STAT1. | lld:pubmed |
pubmed-article:15009724 | pubmed:language | eng | lld:pubmed |
pubmed-article:15009724 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15009724 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15009724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15009724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15009724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15009724 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15009724 | pubmed:month | Feb | lld:pubmed |
pubmed-article:15009724 | pubmed:issn | 0022-202X | lld:pubmed |
pubmed-article:15009724 | pubmed:author | pubmed-author:HeinrichPeter... | lld:pubmed |
pubmed-article:15009724 | pubmed:author | pubmed-author:BehrmannIrisI | lld:pubmed |
pubmed-article:15009724 | pubmed:author | pubmed-author:BosserhoffAnj... | lld:pubmed |
pubmed-article:15009724 | pubmed:author | pubmed-author:KortylewskiMa... | lld:pubmed |
pubmed-article:15009724 | pubmed:author | pubmed-author:KomyodWarapor... | lld:pubmed |
pubmed-article:15009724 | pubmed:author | pubmed-author:KauffmannMari... | lld:pubmed |
pubmed-article:15009724 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15009724 | pubmed:volume | 122 | lld:pubmed |
pubmed-article:15009724 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15009724 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15009724 | pubmed:pagination | 414-22 | lld:pubmed |
pubmed-article:15009724 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:15009724 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15009724 | pubmed:articleTitle | Interferon-gamma-mediated growth regulation of melanoma cells: involvement of STAT1-dependent and STAT1-independent signals. | lld:pubmed |
pubmed-article:15009724 | pubmed:affiliation | Institut für Biochemie, Aachen, Germany. | lld:pubmed |
pubmed-article:15009724 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15009724 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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