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EXPLORING THE ROLE OF NFκB HOMOLOGS IN AUTOPHAGIC CELL DEATH IN THE DROSOPHILA SALIVARY GLAND

dc.contributor.advisorWu, Louisa Pen_US
dc.contributor.authorIvory, Adrienneen_US
dc.date.accessioned2009-07-02T06:03:06Z
dc.date.available2009-07-02T06:03:06Z
dc.date.issued2009en_US
dc.identifier.urihttp://hdl.handle.net/1903/9246
dc.description.abstractThe innate immune response is an ancient, highly conserved means of defense against pathogens. An important mediator of innate immunity is the NF-κB (Nuclear Factor-Kappa B) family of transcription factors. Activation of immune-signaling pathways leads to the nuclear translocation of NFκB proteins which initiate the transcription of antimicrobial peptides (AMPs) that circulate and destroy microbes. In Drosophila, these AMPs are up-regulated during the destruction of larval salivary glands. Salivary gland cells are destroyed via autophagy during metamorphosis. This project sought to determine what, if any, role the NFκB transcription factors have in autophagic cell death. Using the Drosophila model, it was determined that a loss of AMP activity during metamorphosis results in a failure to completely degrade larval salivary glands, and this defect appears to be due to an inability to remove autophagic vacuoles. It is suggested that AMPs may serve to degrade the membranes of autophagic vacuoles.en_US
dc.format.extent2351878 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen_US
dc.titleEXPLORING THE ROLE OF NFκB HOMOLOGS IN AUTOPHAGIC CELL DEATH IN THE DROSOPHILA SALIVARY GLANDen_US
dc.typeThesisen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.contributor.departmentCell Biology & Molecular Geneticsen_US
dc.subject.pqcontrolledBiology, Molecularen_US
dc.subject.pqcontrolledBiology, Geneticsen_US
dc.subject.pqcontrolledBiology, Cellen_US
dc.subject.pquncontrolledantimicrobial peptidesen_US
dc.subject.pquncontrolledautophagyen_US
dc.subject.pquncontrolleddrosophilaen_US
dc.subject.pquncontrolledNF -kappa Ben_US
dc.subject.pquncontrolledsalivary glanden_US


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