The extracellular loop 2 of TM4SF5 inhibits integrin alpha2 on hepatocytes under collagen type I environment

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dc.contributor.authorS A Lee-
dc.contributor.authorY M Kim-
dc.contributor.authorT K Kwak-
dc.contributor.authorH J Kim-
dc.contributor.authorSemi Kim-
dc.contributor.authorW Ko-
dc.contributor.authorS H Kim-
dc.contributor.authorK H Park-
dc.contributor.authorH J Kim-
dc.contributor.authorM Cho-
dc.contributor.authorJ W Lee-
dc.date.accessioned2017-04-19T09:15:39Z-
dc.date.available2017-04-19T09:15:39Z-
dc.date.issued2009-
dc.identifier.issn0143-3334-
dc.identifier.uri10.1093/carcin/bgp234ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9255-
dc.description.abstractFour-transmembrane L6 family member 5 (TM4SF5) and its homolog L6, a tumor antigen, form a four-transmembrane L6 family. TM4SF5 expression causes uncontrolled cell proliferation and angiogenesis. Although other genuine transmembrane 4 superfamily (TM4SF) members co-operate with integrins for cell migration, roles of TM4SF5 in the cellular spreading and migration are unknown. Using hepatocarcinoma cell clones that ectopically express TM4SF5, we found that cross talks via an extracellular interaction between TM4SF5 and integrin α2 in collagen type I environment inhibited integrin α2 functions such as spreading on and migration toward collagen I, which were recovered by suppression of TM4SF5 or structural disturbance of its second extracellular loop using a peptide or mutagenesis. Altogether, the observations suggest that TM4SF5 in hepatocytes negatively regulates integrin α2 function via an interaction between the extracellular loop 2 of TM4SF5 and integrin α2 during cell spreading on and migration through collagen I environment.-
dc.publisherOxford Univ Press-
dc.titleThe extracellular loop 2 of TM4SF5 inhibits integrin alpha2 on hepatocytes under collagen type I environment-
dc.title.alternativeThe extracellular loop 2 of TM4SF5 inhibits integrin alpha2 on hepatocytes under collagen type I environment-
dc.typeArticle-
dc.citation.titleCarcinogenesis-
dc.citation.number11-
dc.citation.endPage1879-
dc.citation.startPage1872-
dc.citation.volume30-
dc.contributor.affiliatedAuthorSemi Kim-
dc.contributor.alternativeName이신애-
dc.contributor.alternativeName김영미-
dc.contributor.alternativeName곽태경-
dc.contributor.alternativeName김현정-
dc.contributor.alternativeName김세미-
dc.contributor.alternativeName고원일-
dc.contributor.alternativeName김성훈-
dc.contributor.alternativeName박기훈-
dc.contributor.alternativeName김현정-
dc.contributor.alternativeName조문재-
dc.contributor.alternativeName이정원-
dc.identifier.bibliographicCitationCarcinogenesis, vol. 30, no. 11, pp. 1872-1879-
dc.identifier.doi10.1093/carcin/bgp234-
dc.description.journalClassY-
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Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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