Modulation of Alzheimer’s Disease related APP Trafficking via Protein Kinase C

Persistent Link:
http://hdl.handle.net/10150/221419
Title:
Modulation of Alzheimer’s Disease related APP Trafficking via Protein Kinase C
Author:
Vithana, Rukmalee
Affiliation:
The University of Arizona College of Medicine - Phoenix
Issue Date:
1-May-2012
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the College of Medicine - Phoenix, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Collection Information:
This item is part of the College of Medicine - Phoenix Scholarly Projects 2012 collection. For more information, contact the Phoenix Biomedical Campus Library at pbc-library@email.arizona.edu.
Publisher:
The University of Arizona.
Abstract:
Chronic phorbol ester treatment treatment of a neuroblastoma cell line, SH-SY5Y, was hypothesized to induce alterations in APP expression and trafficking such that the holoprotein will increasingly localize to mitochondria. Fluorescent immunocytochemistry and confocal microscopy was used primarily to visualize co-localization of Amyloid precursor protein (APP) to Translocase complex of the outer mitochondrial membrane (TOMM machinery) on the mitochondria. Co-localization experiments were inconclusive in showing that chronic phorbol 12-myristate 13- acetate (PMA) treatment affects APP trafficking to mitochondria. Due to those results, mitochondrial gradient fractionation experiments and subsequent western blots were started to determine if there was increased APP expression at the mitochondrial membrane and if protein kinase C (PKC) was activated by chronic PMA treatment.
MeSH Subjects:
Alzheimer Disease; Protein Kinase C; Amyloid Precursor Protein Secretases
Description:
A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Mentor:
Valla, Jon PhD

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleModulation of Alzheimer’s Disease related APP Trafficking via Protein Kinase Cen_US
dc.contributor.authorVithana, Rukmaleeen_US
dc.contributor.departmentThe University of Arizona College of Medicine - Phoenixen_US
dc.date.issued2012-05-01-
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the College of Medicine - Phoenix, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.collectioninformationThis item is part of the College of Medicine - Phoenix Scholarly Projects 2012 collection. For more information, contact the Phoenix Biomedical Campus Library at pbc-library@email.arizona.edu.en_US
dc.publisherThe University of Arizona.en_US
dc.description.abstractChronic phorbol ester treatment treatment of a neuroblastoma cell line, SH-SY5Y, was hypothesized to induce alterations in APP expression and trafficking such that the holoprotein will increasingly localize to mitochondria. Fluorescent immunocytochemistry and confocal microscopy was used primarily to visualize co-localization of Amyloid precursor protein (APP) to Translocase complex of the outer mitochondrial membrane (TOMM machinery) on the mitochondria. Co-localization experiments were inconclusive in showing that chronic phorbol 12-myristate 13- acetate (PMA) treatment affects APP trafficking to mitochondria. Due to those results, mitochondrial gradient fractionation experiments and subsequent western blots were started to determine if there was increased APP expression at the mitochondrial membrane and if protein kinase C (PKC) was activated by chronic PMA treatment.en_US
dc.typeThesisen_US
dc.subject.meshAlzheimer Diseaseen_US
dc.subject.meshProtein Kinase Cen_US
dc.subject.meshAmyloid Precursor Protein Secretasesen_US
dc.descriptionA Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.en_US
dc.contributor.mentorValla, Jon PhDen_US
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