Electronic Theses and Dissertations

Identifier

6518

Maha Attar

Date

2019

Document Type

Thesis

Degree Name

Master of Science

Major

Biology

Committee Chair

Ramin Homayouni

Committee Member

Carlos Estrano

Committee Member

Omar Skalli

Abstract

NIPSNAP1 (4-nitrophenyl phosphatase domain and non-neuronal SNAP25-like protein homolog1) is an evolutionarily conserved mitochondrial protein that interacts with the cytoplasmic domain of the Alzheimer's Disease (AD) amyloid precursor protein (APP). NIPSNAP1 interaction with APP may contribute to mitochondrial dysfunction and possibly to neurodegeneration associated with AD. To investigate the molecular and cellular role of NIPSNAP1, we created a NIPSNAP1 knockdown cell line using shRNA lentiviral strategy. Immunoblot analysis showed that one shRNA construct reduced NIPSNAP1 protein levels by approximately 85%. Reduction of NIPSNAP1 protein required at least 10 days after shRNA lentiviral transduction, suggesting that NIPSNAP1 protein is highly stable in hepatoma cells. In addition, NIPSNAP1 deficiency reduced Reactive Oxygen Species (ROS), suggesting that NIPSNAP1 regulates mitochondrial function. Taken together, this work establishes a NIPSNAP1 knock-down cell line in which detailed molecular and cellular studies can be conducted in the future.

Comments

Data is provided by the student.

Library Comment

Dissertation or thesis originally submitted to the local University of Memphis Electronic Theses & dissertation (ETD) Repository.

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