| pubmed-article:15010535 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C1513095 | lld:lifeskim |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C1148798 | lld:lifeskim |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C1519697 | lld:lifeskim |
| pubmed-article:15010535 | lifeskim:mentions | umls-concept:C1707719 | lld:lifeskim |
| pubmed-article:15010535 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:15010535 | pubmed:dateCreated | 2004-3-25 | lld:pubmed |
| pubmed-article:15010535 | pubmed:abstractText | The notorious resistance of melanoma cells to drug treatment can be overcome by expression of a 50-aa peptide derived from activating transcription factor 2 (ATF2(50-100)). Here we demonstrate that ATF2(50-100) induced apoptosis by sequestering ATF2 to the cytoplasm, thereby inhibiting its transcriptional activities. Furthermore, ATF2(50-100) binds to c-Jun N-terminal kinase (JNK) and increases its activity. Mutation within ATF2(50-100) that impairs association with JNK and the inhibition of JNK or c-Jun expression by RNA interference (RNAi) reduces the degree of ATF2(50-100)-induced apoptosis. In contrast, TAM67, a dominant negative of the Jun family of transcription factors, or JunD RNAi attenuates sensitization of melanoma cells expressing ATF2(50-100) to apoptosis after treatment with anisomycin, which is used as a model drug. Mutations within the JNK binding region of ATF2(50-100) or expression of TAM67 or JunD RNAi attenuates inhibition of melanoma's tumorigenicity by ATF2(50-100). We conclude that inhibition of ATF2 in concert with increased JNK/Jun and JunD activities is central for the sensitization of melanoma cells to apoptosis and inhibition of their tumorigenicity. | lld:pubmed |
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| pubmed-article:15010535 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15010535 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15010535 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15010535 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15010535 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15010535 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:15010535 | pubmed:author | pubmed-author:RonaiZe'evZ | lld:pubmed |
| pubmed-article:15010535 | pubmed:author | pubmed-author:JonesNicN | lld:pubmed |
| pubmed-article:15010535 | pubmed:author | pubmed-author:BhoumikAnindi... | lld:pubmed |
| pubmed-article:15010535 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15010535 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:15010535 | pubmed:volume | 101 | lld:pubmed |
| pubmed-article:15010535 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15010535 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15010535 | pubmed:pagination | 4222-7 | lld:pubmed |
| pubmed-article:15010535 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15010535 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15010535 | pubmed:articleTitle | Transcriptional switch by activating transcription factor 2-derived peptide sensitizes melanoma cells to apoptosis and inhibits their tumorigenicity. | lld:pubmed |
| pubmed-article:15010535 | pubmed:affiliation | Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, NY 10029, USA. | lld:pubmed |
| pubmed-article:15010535 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15010535 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15010535 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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