| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 101 === Severe acute respiratory syndrome (SARS) is a highly infectious disease outbreak suddenly in 2003. SARS coronavirus (SARS-CoV) has been identified as the etiological agent of SARS. We have demonstrated that SARS-CoV indeed expresses a novel protein 3a. We identified presenilin-associated rhomboid-like (PARL), an anti-apoptotic protein, as a protein 3a interaction partner by using yeast-two-hybrid system. The N-terminus of protein 3a and PARL might response for protein bindings between these two molecules. Expression of protein 3a caused cellular apoptosis, and altered the mitochondria membrane potential and subcellular distributions of cytochrome c oxidase subunit 1 (COX1) in Vero E6 cell. Interestingly, protein3a reduced the PARL protein stability and its nuclear signals of β-peptide (53~77 residues of PARL) in Vero E6 cell. These results suggest that protein 3a induces apoptosis might through modulating of PARL. In this thesis, we focus on the characterization of the interactions request for the function of protein 3a-PARL interaction. We demonstrated that protein 3a interacted with PARL by in vitro pull-down assay. The N-terminal trans-membrane regions is important for protein 3a-meditated apoptosis and reducing nuclear signal of β-peptide.
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