{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/78135"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/78135","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Role of X-box Binding Protein 1 in Regulation of Retinal Müller Glia Metabolism","abstract":"M.S.","abstract_html":"M.S.","abstract_has_math":false,"creators":["Kelly, Kristen"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Zhang, Sarah","Neuroscience"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-06-28T20:34:35Z","date_published":"2018-06-28T20:34:35Z","updated_at":"2026-07-27T19:05:09Z","subjects":["neurosciences","ophthalmology","biochemistry"],"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/10477/78135","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Zhang, Sarah","Neuroscience"]},{"key":"dc:creator","label":"Author","values":["Kelly, Kristen"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2018-06-28T20:34:35Z","2018","2018-06-01 15:37:09"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["neurosciences","ophthalmology","biochemistry"]}]},{"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/10477/78135"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["M.S.","Müller glia play a critical role in maintaining retinal homeostasis through shuttling metabolic substrates to and from retinal neurons, releasing trophic factors, regulating neurotransmission, providing structural support, and regulating the extracellular environment. Thus, studying the regulation of Müller glia metabolism could provide helpful insights for understanding retinal dysfunction and degeneration. In this study, we investigate the role of X-box binding protein 1 (XBP1), a stress-inducible transcription factor, in regulation of retinal Müller glial metabolism. We hypothesize that deletion of XBP1 in Müller glia leads to increases in glycolytic capacity, which could in turn alter retinal metabolism. To test this hypothesis, we generated XBP1 conditional knockout (cKO) mice that lack XBP1 specifically in Müller glia using the Cre/LoxP system. Using a Seahorse extracellular flux metabolic analyzer, we measured mitochondrial respiration and glycolysis in the retina and in isolated Müller cells from XBP1 cKO mice. Our results demonstrate an increased rate of glycolysis in XBP1 cKO retinas and in XBP1-deficient Müller cells. These changes are associated with elevated glucose uptake and upregulation of glucose transporters GLUT1 and GLUT2. Additionally, two regulatory enzymes involved in glycolysis, pyruvate kinase and Hexokinase 1, are also upregulated in XBP1 cKO Müller cells. Taken together, our data suggest that XBP1 plays an important role in regulation of glucose metabolism in retinal Müller glia, which, although consisting of a relatively small population of retinal cells, could consequently influence retinal metabolic profile and function."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Role of X-box Binding Protein 1 in Regulation of Retinal Müller Glia Metabolism"]}]}],"canonical_facts":{"dc:contributor":["Zhang, Sarah","Neuroscience"],"dc:creator":["Kelly, Kristen"],"dc:date":["2018-06-28T20:34:35Z","2018","2018-06-01 15:37:09"],"dc:description":["M.S.","Müller glia play a critical role in maintaining retinal homeostasis through shuttling metabolic substrates to and from retinal neurons, releasing trophic factors, regulating neurotransmission, providing structural support, and regulating the extracellular environment. Thus, studying the regulation of Müller glia metabolism could provide helpful insights for understanding retinal dysfunction and degeneration. In this study, we investigate the role of X-box binding protein 1 (XBP1), a stress-inducible transcription factor, in regulation of retinal Müller glial metabolism. We hypothesize that deletion of XBP1 in Müller glia leads to increases in glycolytic capacity, which could in turn alter retinal metabolism. To test this hypothesis, we generated XBP1 conditional knockout (cKO) mice that lack XBP1 specifically in Müller glia using the Cre/LoxP system. Using a Seahorse extracellular flux metabolic analyzer, we measured mitochondrial respiration and glycolysis in the retina and in isolated Müller cells from XBP1 cKO mice. Our results demonstrate an increased rate of glycolysis in XBP1 cKO retinas and in XBP1-deficient Müller cells. These changes are associated with elevated glucose uptake and upregulation of glucose transporters GLUT1 and GLUT2. Additionally, two regulatory enzymes involved in glycolysis, pyruvate kinase and Hexokinase 1, are also upregulated in XBP1 cKO Müller cells. Taken together, our data suggest that XBP1 plays an important role in regulation of glucose metabolism in retinal Müller glia, which, although consisting of a relatively small population of retinal cells, could consequently influence retinal metabolic profile and function."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/78135"],"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":["neurosciences","ophthalmology","biochemistry"],"dc:title":["Role of X-box Binding Protein 1 in Regulation of Retinal Müller Glia Metabolism"],"dc:type":["Text","Thesis"]},"updated_at":"2026-07-27T19:05:09Z"}