{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/39117"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/39117","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"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":"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.","abstract_html":"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.","abstract_has_math":false,"creators":["Lenhausen, Audrey May"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013","date_published":"2013","updated_at":"2026-07-27T22:01:39Z","subjects":[],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/39117","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Lenhausen, Audrey May"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2014-01-15T09:35:21Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2014-07-15T08:30:09Z"]},{"key":"dc:date.issued","label":"Date","values":["2013"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/39117"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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."]},{"key":"dc:title","label":"Title","values":["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"]}]}],"canonical_facts":{"dc:creator":["Lenhausen, Audrey May"],"dc:date.accessioned":["2014-01-15T09:35:21Z"],"dc:date.available":["2014-07-15T08:30:09Z"],"dc:date.issued":["2013"],"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."],"dc:identifier.uri":["http://hdl.handle.net/10339/39117"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:title":["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"],"dc:type":["Dissertation"]},"updated_at":"2026-07-27T22:01:39Z"}