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Genetic Analysis of Ninjurin A, A stress-regulated potein that induces nonapoptotic cell death

dc.creatorBroderick, Sarah M
dc.date.accessioned2020-08-22T00:36:04Z
dc.date.available2013-04-19
dc.date.issued2013-04-19
dc.identifier.urihttps://etd.library.vanderbilt.edu/etd-04182013-154535
dc.identifier.urihttp://hdl.handle.net/1803/12192
dc.description.abstractNinjurins are a conserved family of transmembrane proteins that increase expression in response to injury and stress. There are few in vivo studies of Ninjurin, and little is known about Ninjurin function. In this thesis I investigated the immune function of a recently generated null mutant of NijA, which did not display a detectable phenotype. Expression studies of the NijA protein show redistribution to the cell surface in larval immune tissues after septic injury. The NijA protein is also upregulated by constitutive activation of the Toll pathway. Ectopic expression of NijA induced cell death. These dying cells appeared to die by nonapoptotic cell death because they did not display hallmarks of apoptotic cells including TUNEL staining and inhibition by p35. Preliminary studies investigating UV-irradiation induced cell death in the NijA null mutant suggests that NijA maybe required to induce stress-activated cell death. These results suggest a role for NijA in stress-activated nonapoptoic cell death.
dc.format.mimetypeapplication/pdf
dc.subjectCell Biology
dc.titleGenetic Analysis of Ninjurin A, A stress-regulated potein that induces nonapoptotic cell death
dc.typedissertation
dc.contributor.committeeMemberHeather Broihier
dc.contributor.committeeMemberEthan Lee
dc.contributor.committeeMemberJulian Hillyer
dc.contributor.committeeMemberLaura Lee
dc.contributor.committeeMemberAndrea Page-McCaw
dc.type.materialtext
thesis.degree.namePHD
thesis.degree.leveldissertation
thesis.degree.disciplineCell and Developmental Biology
thesis.degree.grantorVanderbilt University
local.embargo.terms2013-04-19
local.embargo.lift2013-04-19
dc.contributor.committeeChairDavid Miller


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