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dc.contributor.advisorBooth, Rachell
dc.contributor.authorLee, Esther
dc.date.accessioned2017-04-10T18:31:45Z
dc.date.available2017-04-10T18:31:45Z
dc.date.created2014-12
dc.date.issued2014-11-19
dc.date.submittedDecember 2014
dc.identifier.urihttps://digital.library.txstate.edu/handle/10877/6554
dc.description.abstractMaintaining homeostasis is crucial for perpetuating good health. Any imbalance, such as hypertension, can lead to heart and kidney disease. Epithelial sodium channels, also known as ENaC, constitute the rate-limiting step of sodium reabsorption in the distal tubules of the nephron in the kidneys. It is here the final, yet critical, 3% to 5% of sodium reabsorption that dictates blood pressure occurs. In this study, β-ENaC was cloned into pESC-Leu and pESC-Leu/γ in order to further characterize accessory proteins in yeast screens using the heterotrimeric channel. An antibody screen against the subunits of ENaC was then performed using Murine Principle Kidney Cortical Collecting Duct (mpkCCD) cells as a means of identifying a primary antibody for western blotting. RNA Interference studies in mpkCCD cells were also performed. Knockdown of the accessory proteins TMED2 and TMP21 through RNAi indicated a decrease in ENaC expression. These results indicated that TMED2 and TMP21 are essential for ENaC trafficking.
dc.formatText
dc.format.extent60 pages
dc.format.medium1 file (.pdf)
dc.language.isoen_US
dc.subjectENaC
dc.subjectAccessory proteins
dc.subjectTMED2
dc.subjectTMP21
dc.subjectmpkCCD cells
dc.titleThe Effects of Accessory Proteins on ENaC Function
txstate.documenttypeThesis
dc.contributor.committeeMemberDavid, Wendi
dc.contributor.committeeMemberLewis, Kevin
thesis.degree.departmentChemistry and Biochemistry
thesis.degree.disciplineBiochemistry
thesis.degree.grantorTexas State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science
txstate.departmentChemistry and Biochemistry


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