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dc.contributor.authorMohd Yusof, Baharuddin
dc.date.accessioned2009-11-13T01:54:47Z
dc.date.available2009-11-13T01:54:47Z
dc.date.issued2009-10-11
dc.identifier.citationp.1A7 1 - 1A7 4en_US
dc.identifier.urihttp://dspace.unimap.edu.my/123456789/7267
dc.descriptionOrganized by School of Mechatronic Engineering (UniMAP) & co-organized by The Institution of Engineering Malaysia (IEM), 11th - 13th October 2009 at Batu Feringhi, Penang, Malaysia.en_US
dc.description.abstractCaspase activated deoxyribonuclease (CAD) is the protein that transmit nuclear localization signal which will induced DNA fragmentation. Both CAD and its inhibitor ICAD is the key for apoptosis. As CAD is binding on RNA, ICAD-L will bind to its budding chain improving the folding. Once CAD synthesis is done, ICAD-L will still bind with CAD forming DFF which is the CAD: ICAD complex. On the contrary, ICAD-S couldn’t bind with CAD budding chain, therefore do not form DFF. When Caspase-3 is activated downstream in Caspase-3 Cascade, ICAD-L will cleaved and release active CAD to degrade DNA.en_US
dc.description.sponsorshipTechnical sponsored by IEEE Malaysia Sectionen_US
dc.language.isoenen_US
dc.publisherUniversiti Malaysia Perlisen_US
dc.relation.ispartofseriesProceedings of the International Conference on Man-Machine Systems (ICoMMS 2009)en_US
dc.subjectCaspase activated deoxyribonuclease (CAD)en_US
dc.subjectICADen_US
dc.subjectDNA fragmentationen_US
dc.subjectApoptosisen_US
dc.subjectCaspase-3en_US
dc.titleComputational modeling of Caspase activated DNAase (CAD) regulation towards Apoptosisen_US
dc.typeWorking Paperen_US


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