pubmed-article:18361917 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18361917 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
pubmed-article:18361917 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:18361917 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:18361917 | lifeskim:mentions | umls-concept:C1825069 | lld:lifeskim |
pubmed-article:18361917 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18361917 | pubmed:dateCreated | 2008-4-15 | lld:pubmed |
pubmed-article:18361917 | pubmed:abstractText | Human ESX1 is a 65-kilodalton (kDa) paired-like homeoprotein that is proteolytically processed into N-terminal 45-kDa and C-terminal 20-kDa fragments. The N-terminal ESX1 fragment, which contains the homeodomain, localizes to the nucleus and represses mRNA transcription from the K-ras gene. When we inoculated human colorectal carcinoma HCT116 constitutive expressing N-terminal region of ESX1 (N-ESX1) into nude mice, transfectant cells uniformly showed decreased tumor-forming activity compared with that of the parental cells. Furthermore, pretreatment of HCT116 carcinoma cells with a fusion protein consisting of N-ESX1 and the protein-transduction domain derived from the human immunodeficiency virus type-1 TAT protein gave rise to a dramatic reduction in the tumorigenicity of HCT116 cells in nude mice. Our results provide first in vivo evidence for the molecular targeting therapeutic application of the K-ras repressor ESX1, especially TAT-mediated transduction of N-ESX1, in the treatment of human cancers having oncogenic K-ras mutations. | lld:pubmed |
pubmed-article:18361917 | pubmed:language | eng | lld:pubmed |
pubmed-article:18361917 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18361917 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18361917 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18361917 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18361917 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18361917 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18361917 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18361917 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18361917 | pubmed:month | May | lld:pubmed |
pubmed-article:18361917 | pubmed:issn | 1090-2104 | lld:pubmed |
pubmed-article:18361917 | pubmed:author | pubmed-author:HatakeyamaMas... | lld:pubmed |
pubmed-article:18361917 | pubmed:author | pubmed-author:KoikeTakaoT | lld:pubmed |
pubmed-article:18361917 | pubmed:author | pubmed-author:IshikawaSusum... | lld:pubmed |
pubmed-article:18361917 | pubmed:author | pubmed-author:YanagiharaMas... | lld:pubmed |
pubmed-article:18361917 | pubmed:author | pubmed-author:HamadaJun-Ich... | lld:pubmed |
pubmed-article:18361917 | pubmed:author | pubmed-author:NakajimaJunta... | lld:pubmed |
pubmed-article:18361917 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18361917 | pubmed:day | 23 | lld:pubmed |
pubmed-article:18361917 | pubmed:volume | 370 | lld:pubmed |
pubmed-article:18361917 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18361917 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18361917 | pubmed:pagination | 189-94 | lld:pubmed |
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pubmed-article:18361917 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18361917 | pubmed:articleTitle | Anti-tumor activity of ESX1 on cancer cells harboring oncogenic K-ras mutation. | lld:pubmed |
pubmed-article:18361917 | pubmed:affiliation | Division of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060-0815, Japan. | lld:pubmed |
pubmed-article:18361917 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18361917 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |