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Wake Forest University

THE PROSURVIVAL ACTIVITIES OF APOPTOSIS-INDUCING FACTOR CONVERGE UPON THE REGULATION OF MITOCHONDRIAL METABOLISM, A NOVEL CELL DEATH PATHWAY, AND THE PROGRESSION OF PROSTATE CANCER

Abstract

dc:description.abstract

Apoptosis-inducing factor (AIF) is a mitochondrial NADH-oxidase originally discovered for its ability to trigger apoptosis through chromatin condensation and DNA cleavage. Although AIF is recognized for its apoptotic function, AIF-mediated cell death has emerged as an atypical cell death pathway; and accumulating evidence indicates AIF to play a more significant role in cell survival by maintaining mitochondrial homeostasis. A loss in AIF protein leads to a variety of mitochondria-specific alterations, including defects in mitochondrial structure, alteration to mitochondrial fission and fusion dynamics, and decreases to the protein complement of the electron transport chain resulting in diminished oxidative phosphorylation. Along with the ability to promote healthy mitochondrial function, AIF has demonstrated a supportive role in cancer cell growth which may be connected to its ability to regulate mitochondrial metabolism. The mechanisms governing how AIF impacts various mitochondrial features are unknown, and a concomitant role for deregulated AIF activity in human disease, in particular cancer, is poorly defined.

Degree

thesis:*
Grantor dc:publisher
Wake Forest University
Year dc:date.issued
2013

Author and committee

dc:creator, dc:contributor.*
Author dc:creator
  • Lenhausen, Audrey May

Rights

Language dc:language.iso
en

Identifiers

dc:identifier.*
Handle dc:identifier.uri
http://hdl.handle.net/10339/39117
OAI identifier oai:identifier
oai:wakespace.lib.wfu.edu:10339/39117

Chain of custody

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Wake Forest University
Base URL
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Last updated
2026-07-27
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OAI-PMH GetRecord
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citation

Lenhausen, Audrey May. THE PROSURVIVAL ACTIVITIES OF APOPTOSIS-INDUCING FACTOR CONVERGE UPON THE REGULATION OF MITOCHONDRIAL METABOLISM, A NOVEL CELL DEATH PATHWAY, AND THE PROGRESSION OF PROSTATE CANCER. Wake Forest University, 2013. http://hdl.handle.net/10339/39117