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Membrane proteins involved in epithelial-mesenchymal transition and tumor invasion: Studies on TMPRSS4 and TM4SF5

DC Field Value Language
dc.contributor.authorKim, Semi-
dc.contributor.authorLee, Jung Weon-
dc.date.accessioned2024-05-29T01:28:10Z-
dc.date.available2024-05-29T01:28:10Z-
dc.date.created2017-11-01-
dc.date.issued2014-03-
dc.identifier.citationGenomics & Informatics, Vol.12 No.1, pp.12-20-
dc.identifier.issn1598-866X-
dc.identifier.urihttps://hdl.handle.net/10371/203877-
dc.description.abstractThe epithelial-mesenchymal transition (EMT) is one mechanism by which cells with mesenchymal features can be generatedand is a fundamental event in morphogenesis. Recently, invasion and metastasis of cancer cells from the primary tumor arenow thought to be initiated by the developmental process termed the EMT, whereby epithelial cells lose cell polarity andcell-cell interactions, and gain mesenchymal phenotypes with increased migratory and invasive properties. The EMT isbelieved to be an important step in metastasis and is implicated in cancer progression, although the influence of the EMT inclinical specimens has been debated. This review presents the recent results of two cell surface proteins, the functions andunderlying mechanisms of which have recently begun to be demonstrated, as novel regulators of the molecular networksthat induce the EMT and cancer progression.-
dc.language영어-
dc.publisher한국유전체학회-
dc.titleMembrane proteins involved in epithelial-mesenchymal transition and tumor invasion: Studies on TMPRSS4 and TM4SF5-
dc.typeArticle-
dc.identifier.doi10.5808/GI.2014.12.1.12-
dc.citation.journaltitleGenomics & Informatics-
dc.citation.endpage20-
dc.citation.number1-
dc.citation.startpage12-
dc.citation.volume12-
dc.identifier.kciidART001866754-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorLee, Jung Weon-
dc.type.docTypeArticle-
dc.description.journalClass2-
dc.subject.keywordAuthorepithelial-mesenchymal transition-
dc.subject.keywordAuthorinvasion-
dc.subject.keywordAuthormembrane proteins-
dc.subject.keywordAuthorTM4SF5-
dc.subject.keywordAuthorTMPRSS4-
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