dc.contributor.authorMeroshini, M.
dc.date.accessioned2016-05-23T07:25:13Z
dc.date.available2016-05-23T07:25:13Z
dc.date.issued2016
dc.identifier.urihttp://hdl.handle.net/10356/67927
dc.description.abstractThe gradual and inevitable process of aging can lead to detrimental effects such as disruptions in cellular processes and accumulation of damage in cells. It has been shown that the number of alternatively spliced genes significantly increases with age, and that aberrant splicing is one of the major causes of a few age-related diseases such as Hutchinson-Gilford progeria syndrome (HGPS), frontotemporal lobar degeneration (FTLD), or Alzheimer's disease (AD). Identification of the key players in splicing can lead to a better understanding of the relationship between aberrant splicing and cardiac aging. One essential component of the splicing process is SRPK2, a member of the the Serine-Arginine Rich Protein Kinase (SRPK) family. A thorough understanding of SRPK2, its interactors, its regulatory mechanism, and its functions the aim of this project. With methods such as BioID proximity labelling, western blots, immunoprecipitation and real time PCR, a few possible interactors of SRPK2 have been short listed, and the regulatory mechanism of SRPK2 cellular levels have been proposed.en_US
dc.format.extent36 p.en_US
dc.language.isoenen_US
dc.rightsNanyang Technological University
dc.subjectDRNTU::Scienceen_US
dc.titleLinking aberrant splicing to cardiac aging : unravelling SRPK2en_US
dc.typeFinal Year Project (FYP)en_US
dc.contributor.supervisorColin Stewarten_US
dc.contributor.schoolSchool of Biological Sciencesen_US
dc.description.degreeBachelor of Science in Biological Sciencesen_US
dc.contributor.organizationA*STAR Institute of Medical Biologyen_US


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