Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/143312
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dc.titleTHE ROLE OF HELICOBACTER PYLORI IN DISRUPTION OF CELL - CELL JUNCTIONS OF GASTRIC EPITHELIAL CELLS
dc.contributor.authorAMITA SEKAR
dc.date.accessioned2018-06-19T18:01:14Z
dc.date.available2018-06-19T18:01:14Z
dc.date.issued2016-01-22
dc.identifier.citationAMITA SEKAR (2016-01-22). THE ROLE OF HELICOBACTER PYLORI IN DISRUPTION OF CELL - CELL JUNCTIONS OF GASTRIC EPITHELIAL CELLS. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/143312
dc.description.abstractH. PYLORI, THE MAJOR ETIOLOGICAL AGENT OF VARIOUS GASTRODUODENAL DISEASES, IS KNOWN TO CAUSE TIGHT JUNCTION DISRUPTION. HOWEVER, THE MECHANISM REMAINS HIGHLY ELUSIVE. THIS STUDY AIMS TO ELUCIDATE THE ROLE OF H. PYLORI IN DISRUPTING GASTRIC EPITHELIAL CELL-CELL JUNCTIONS. THIS STUDY SHOWS THAT H. PYLORI PLAYS AN ESSENTIAL ROLE IN DELOCALIZING THE TIGHT JUNCTION PROTEINS RESULTING IN THE DISRUPTION OF CELL-CELL JUNCTIONS WITH AN ACTIVE INVOLVEMENT OF MAPK/ERK PATHWAY AND HPGGT. TRANSCRIPTOMIC AND EPIGENETIC ANALYSES FURTHER ESTABLISHED THE ROLE OF H. PYLORI IN REGULATING CELL JUNCTION ASSEMBLY AND MAPK CASCADE, CONTRIBUTING TO HOST PATHOGENESIS. THESE FINDINGS SHED MORE LIGHT INTO OUR UNDERSTANDING OF COMPLEX HOST-PATHOGEN INTERACTIONS WHEREIN THE INTERPLAY OF ACTIVATED HOST SIGNALLING MOLECULES AND BACTERIAL VIRULENCE FACTORS INDUCE CELL JUNCTION DISRUPTION.
dc.language.isoen
dc.subjectHelicobacter pylori, Cell-cell junctions, MAPK/ERK, GGT, Epigenetics, Endogenous Retroviruses
dc.typeThesis
dc.contributor.departmentMICROBIOLOGY & IMMUNOLOGY
dc.contributor.supervisorHO BOW
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
Appears in Collections:Ph.D Theses (Open)

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