dc.contributor.authorLim, Wan'e.
dc.date.accessioned2009-05-14T02:01:31Z
dc.date.available2009-05-14T02:01:31Z
dc.date.copyright2009en_US
dc.date.issued2009
dc.identifier.urihttp://hdl.handle.net/10356/15684
dc.description.abstractSerum Amyloid A (SAA) is known to be important in atherogenesis although the mechanisms are unclear. It is shown to promote cholesterol efflux activity of cells in several studies and may prevent atherosclerosis by promoting cholesterol efflux in foam cells of the atherosclerotic lesions. Therefore, it is important to elucidate the mechanism of SAA-mediated cholesterol efflux. Human Embryonic Kidney (HEK) 293 cells were first transfected to produce endogenous wild type SAA1.1, mutated SAA1.1 without the N-terminal lipid binding domain and mutated SAA1.1 with an amino acid substitution of Glycine to Aspartic acid at the 8th amino acid. The SAA1.1 concentration in cells and culture medium were measured with Enzyme-linked immunosorbent assay (ELISA) to determine SAA1.1 expression. After transfected cells were labeled with 3H cholesterol, their cholesterol effluxes were determined by measuring the radioactivity of cell lysate and culture medium. The results showed that secreted SAA1.1 promoted a significant increase in cholesterol efflux activity of HEK293 cells. The signal peptide of SAA1.1 was also demonstrated to be important for protein secretion. Hence, secreted SAA1.1 is shown to promote cholesterol efflux through its interaction at cell membrane in this study.en_US
dc.format.extent26 p.en_US
dc.language.isoenen_US
dc.rightsNanyang Technological University
dc.subjectDRNTU::Science::Biological sciences::Molecular biologyen_US
dc.titleEffects of wild type Serum Amyloid A1.1 and its derivative proteins on the cholesterol efflux activity.en_US
dc.typeFinal Year Project (FYP)en_US
dc.description.degreeBachelor of Science in Biological Sciencesen_US
dc.contributor.organizationNational University of Singaporeen_US
dc.contributor.supervisor2Heng, Chew Kiaten_US


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