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dc.contributor.authorTai, Chun Sanen_US
dc.contributor.authorChen, Yi Yunen_US
dc.contributor.authorChen, Wen Liangen_US
dc.date.accessioned2019-04-03T06:37:00Z-
dc.date.available2019-04-03T06:37:00Z-
dc.date.issued2016-01-01en_US
dc.identifier.issn2314-6133en_US
dc.identifier.urihttp://dx.doi.org/10.1155/2016/7123587en_US
dc.identifier.urihttp://hdl.handle.net/11536/132912-
dc.description.abstractbeta-Lactoglobulin (LG) is suspected to enhance ormodulate humanimmune responses. Moreover, LGis also hypothesized to increase human cell proliferation. However, these potential functions of LG have not been directly or thoroughly addressed. In this study, we demonstrated that LG is a potent stimulator of cell proliferation using a hybridoma cell (a splenocyte fused with amyeloma cell) model. LG's ability to promote cell proliferation was lost when the protein is denatured. To further investigate the influence of LG's conformation on cell proliferation, we chemically modified LG by either carboxymethylation (CM) or acetylation and observed significantly reduced cell proliferation when the protein structure was altered. Furthermore, we proved that LG enhances cell proliferation via receptor-mediated membrane IgM receptor. These data indicated that nondenatured LG is the major component in milk that modulates cell proliferation. Collectively, our study showed that LG plays a key role in enhancing immune responses by promoting cell proliferation through IgM receptor.en_US
dc.language.isoen_USen_US
dc.titlebeta-Lactoglobulin Influences Human Immunity and Promotes Cell Proliferationen_US
dc.typeArticleen_US
dc.identifier.doi10.1155/2016/7123587en_US
dc.identifier.journalBIOMED RESEARCH INTERNATIONALen_US
dc.citation.spage0en_US
dc.citation.epage0en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000388849500001en_US
dc.citation.woscount2en_US
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