{"id":{"repo_id":"york","oai_identifier":"oai:yorkspace.library.yorku.ca:10315/35455"},"canonical_url":"https://search.dev.ndltd.org/etd/york/oai:yorkspace.library.yorku.ca:10315/35455","repository":{"repo_id":"york","name":"York University","base_url":"https://yorkspace.library.yorku.ca/oai/request"},"display":{"title":"A Novel Protective Role for p130 in Neuron Oxidative Stress","abstract":"The human brain is the most energy-consuming and highly oxidative organ in the body. It generates high levels of mitochondrial reactive oxygen species (ROS), damaging proteins and DNA. This is evident in neurodegenerative diseases and aging where the brains defence mechanisms prove insufficient. We provide insight into a novel mechanism of ROS defence in the brain, mediated via p130 that limits oxidative phosphorylation. Conditions of increased metabolic stress or treatment of neurons with ROS inducing agent resulted in mitochondrial localization of p130 in neurons. In the mitochondria, p130 bound to mitochondrial DNA and was associated with decreased mitochondrial gene expression. This resulted in decreased ATP production, thus limiting ROS generation. Our results highlight a new understanding of transcriptional regulation of the mitochondrial genome by the nuclear transcriptional corepressor p130. This might serve as a potential mechanism to control ROS production of neurons in response to increased metabolic stress.","abstract_html":"The human brain is the most energy-consuming and highly oxidative organ in the body. It generates high levels of mitochondrial reactive oxygen species (ROS), damaging proteins and DNA. This is evident in neurodegenerative diseases and aging where the brains defence mechanisms prove insufficient. We provide insight into a novel mechanism of ROS defence in the brain, mediated via p130 that limits oxidative phosphorylation. Conditions of increased metabolic stress or treatment of neurons with ROS inducing agent resulted in mitochondrial localization of p130 in neurons. In the mitochondria, p130 bound to mitochondrial DNA and was associated with decreased mitochondrial gene expression. This resulted in decreased ATP production, thus limiting ROS generation. Our results highlight a new understanding of transcriptional regulation of the mitochondrial genome by the nuclear transcriptional corepressor p130. This might serve as a potential mechanism to control ROS production of neurons in response to increased metabolic stress.","abstract_has_math":false,"creators":["D'Souza, Ninoschka Carolyn Mervyn"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Scime, Anthony"],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-11-21","date_published":"2018-11-21","updated_at":"2026-07-24T06:34:03Z","subjects":["Cellular biology"],"languages":["en"],"rights":["Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10315/35455","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Scime, Anthony"]},{"key":"dc:creator","label":"Author","values":["D'Souza, Ninoschka Carolyn Mervyn"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2018-11-21T13:37:26Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2018-11-21T13:37:26Z"]},{"key":"dc:date.issued","label":"Date","values":["2018-11-21"]},{"key":"dc:type","label":"Dc Type","values":["Electronic Thesis or Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Cellular biology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10315/35455"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The human brain is the most energy-consuming and highly oxidative organ in the body. It generates high levels of mitochondrial reactive oxygen species (ROS), damaging proteins and DNA. This is evident in neurodegenerative diseases and aging where the brains defence mechanisms prove insufficient. We provide insight into a novel mechanism of ROS defence in the brain, mediated via p130 that limits oxidative phosphorylation. Conditions of increased metabolic stress or treatment of neurons with ROS inducing agent resulted in mitochondrial localization of p130 in neurons. In the mitochondria, p130 bound to mitochondrial DNA and was associated with decreased mitochondrial gene expression. This resulted in decreased ATP production, thus limiting ROS generation. Our results highlight a new understanding of transcriptional regulation of the mitochondrial genome by the nuclear transcriptional corepressor p130. This might serve as a potential mechanism to control ROS production of neurons in response to increased metabolic stress."]},{"key":"dc:title","label":"Title","values":["A Novel Protective Role for p130 in Neuron Oxidative Stress"]}]}],"canonical_facts":{"dc:contributor.advisor":["Scime, Anthony"],"dc:creator":["D'Souza, Ninoschka Carolyn Mervyn"],"dc:date.accessioned":["2018-11-21T13:37:26Z"],"dc:date.available":["2018-11-21T13:37:26Z"],"dc:date.issued":["2018-11-21"],"dc:description.abstract":["The human brain is the most energy-consuming and highly oxidative organ in the body. It generates high levels of mitochondrial reactive oxygen species (ROS), damaging proteins and DNA. This is evident in neurodegenerative diseases and aging where the brains defence mechanisms prove insufficient. We provide insight into a novel mechanism of ROS defence in the brain, mediated via p130 that limits oxidative phosphorylation. Conditions of increased metabolic stress or treatment of neurons with ROS inducing agent resulted in mitochondrial localization of p130 in neurons. In the mitochondria, p130 bound to mitochondrial DNA and was associated with decreased mitochondrial gene expression. This resulted in decreased ATP production, thus limiting ROS generation. Our results highlight a new understanding of transcriptional regulation of the mitochondrial genome by the nuclear transcriptional corepressor p130. This might serve as a potential mechanism to control ROS production of neurons in response to increased metabolic stress."],"dc:identifier.uri":["http://hdl.handle.net/10315/35455"],"dc:language.iso":["en"],"dc:rights":["Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests."],"dc:subject":["Cellular biology"],"dc:title":["A Novel Protective Role for p130 in Neuron Oxidative Stress"],"dc:type":["Electronic Thesis or Dissertation"]},"updated_at":"2026-07-24T06:34:03Z"}