{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/80829"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/80829","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"The Role of APOBEC3 A/G-induced RNA Editing in Stress Response of Immune cells","abstract":"Ph.D.","abstract_html":"Ph.D.","abstract_has_math":false,"creators":["Alqassim, Emad; 0000-0003-0765-7569"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Segal, Brahm","Roswell Park"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-10-29T16:47:21Z","date_published":"2019-10-29T16:47:21Z","updated_at":"2026-07-27T19:05:25Z","subjects":["immunology","pathology","cancer prevention and control"],"languages":["eng"],"rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10477/80829","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Segal, Brahm","Roswell Park"]},{"key":"dc:creator","label":"Author","values":["Alqassim, Emad; 0000-0003-0765-7569"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-10-29T16:47:21Z","2019","2019-06-05 10:23:29"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["immunology","pathology","cancer prevention and control"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/10477/80829"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Ph.D.","Project: Macrophages acquire proinflammatory M1 phenotype in response to microbial products or proinflammatory cytokines such as IFN-g, TNF and TLR ligands. However, intracellular mechanisms mediating M1 polarization are incompletely understood. We recently described identification APOBEC3A-mediated cellular site-specific C-to-U RNA editing in M1 macrophages. However, the functional significance of this RNA editing is uncertain. Here, we show that RNA editing in macrophages is also induced by viral infections including adenovirus, influenza, and Maraba viruses. Knockdown (KD) of A3A impairs cellular RNA editing and alters M1-related gene expression and cytokine secretion patterns. RNA-Seq analysis shows that A3A causes protein recoding RNA editing in dozens of genes, including novel highly edited (>50%) genes THOC5 and ZNF124A during M1 polarization. A3A KD reduces expression of IL6, IL23A, IL12B genes, surface protein expression of CD86 and the secretion of proinflammatory cytokines IL-1b and TNFa in M1 macrophages. KD of A3A increases glycolysis and glycolytic capacity. These results demonstrate that induction of RNA editing by A3A is required for optimum polarization of proinflammatory macrophages and that epitranscriptomic enzymatic recoding plays a role in macrophage phenotype plasticity. Project 2BackgroundProtein recoding by RNA editing is required for normal health and evolutionary adaptation. However, de novo induction of RNA editing in response to environmental factors is an uncommon phenomenon. While APOBEC3A edits many mRNAs in monocytes and macrophages in response to hypoxia and interferons, the physiological significance of such editing is unclear. Results: Here, we show that the related cytidine deaminase, APOBEC3G, induces site-specific C-to-U RNA editing in natural killer cells, lymphoma cell lines, and, to a lesser extent, CD8-positive T cells upon cellular crowding and hypoxia."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The Role of APOBEC3 A/G-induced RNA Editing in Stress Response of Immune cells"]}]}],"canonical_facts":{"dc:contributor":["Segal, Brahm","Roswell Park"],"dc:creator":["Alqassim, Emad; 0000-0003-0765-7569"],"dc:date":["2019-10-29T16:47:21Z","2019","2019-06-05 10:23:29"],"dc:description":["Ph.D.","Project: Macrophages acquire proinflammatory M1 phenotype in response to microbial products or proinflammatory cytokines such as IFN-g, TNF and TLR ligands. However, intracellular mechanisms mediating M1 polarization are incompletely understood. We recently described identification APOBEC3A-mediated cellular site-specific C-to-U RNA editing in M1 macrophages. However, the functional significance of this RNA editing is uncertain. Here, we show that RNA editing in macrophages is also induced by viral infections including adenovirus, influenza, and Maraba viruses. Knockdown (KD) of A3A impairs cellular RNA editing and alters M1-related gene expression and cytokine secretion patterns. RNA-Seq analysis shows that A3A causes protein recoding RNA editing in dozens of genes, including novel highly edited (>50%) genes THOC5 and ZNF124A during M1 polarization. A3A KD reduces expression of IL6, IL23A, IL12B genes, surface protein expression of CD86 and the secretion of proinflammatory cytokines IL-1b and TNFa in M1 macrophages. KD of A3A increases glycolysis and glycolytic capacity. These results demonstrate that induction of RNA editing by A3A is required for optimum polarization of proinflammatory macrophages and that epitranscriptomic enzymatic recoding plays a role in macrophage phenotype plasticity. Project 2BackgroundProtein recoding by RNA editing is required for normal health and evolutionary adaptation. However, de novo induction of RNA editing in response to environmental factors is an uncommon phenomenon. While APOBEC3A edits many mRNAs in monocytes and macrophages in response to hypoxia and interferons, the physiological significance of such editing is unclear. Results: Here, we show that the related cytidine deaminase, APOBEC3G, induces site-specific C-to-U RNA editing in natural killer cells, lymphoma cell lines, and, to a lesser extent, CD8-positive T cells upon cellular crowding and hypoxia."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/80829"],"dc:language":["eng"],"dc:publisher":["State University of New York at Buffalo"],"dc:rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"dc:subject":["immunology","pathology","cancer prevention and control"],"dc:title":["The Role of APOBEC3 A/G-induced RNA Editing in Stress Response of Immune cells"],"dc:type":["Text","Dissertation"]},"updated_at":"2026-07-27T19:05:25Z"}