{"id":{"repo_id":"nus","oai_identifier":"oai:scholarbank.nus.edu.sg:10635/28325"},"canonical_url":"https://search.dev.ndltd.org/etd/nus/oai:scholarbank.nus.edu.sg:10635/28325","repository":{"repo_id":"nus","name":"National University of Singapore","base_url":"https://scholarbank.nus.edu.sg/oai/request"},"display":{"title":"Role of Abberant Proteolysis in the Pathogenesis of APL","abstract":"Acute promyelocytic leukemia (APL), a subtype of acute myeloid leukemia (AML), is caused by PML-RARN1, a fusion protein resulting from chromosomal translocation involving the promyelocytic leukemia (PML) and the retinoic acid receptor N1 (RARN1) genes. PML-RARN1 promotes misfolding of nuclear hormone receptor corepressor (N-CoR) and that accumulation of misfolded N-CoR in the ER induces endoplasmic reticulum (ER) stress and activates unfolded protein response (UPR). Although accumulation of misfolded proteins is known to trigger UPR-induced cytotoxic cell death in several neurodegenerative disorders, APL cells are notably resistant to UPR-induced apoptosis. This project was initiated with the goals to investigate how N-CoR misfolding supports the survival and growth of APL cells, and to screen potential therapeutic agents that could induce growth arrest through targeting the misfolded N-CoR-induced survival pathways in APL.","abstract_html":"Acute promyelocytic leukemia (APL), a subtype of acute myeloid leukemia (AML), is caused by PML-RARN1, a fusion protein resulting from chromosomal translocation involving the promyelocytic leukemia (PML) and the retinoic acid receptor N1 (RARN1) genes. PML-RARN1 promotes misfolding of nuclear hormone receptor corepressor (N-CoR) and that accumulation of misfolded N-CoR in the ER induces endoplasmic reticulum (ER) stress and activates unfolded protein response (UPR). Although accumulation of misfolded proteins is known to trigger UPR-induced cytotoxic cell death in several neurodegenerative disorders, APL cells are notably resistant to UPR-induced apoptosis. This project was initiated with the goals to investigate how N-CoR misfolding supports the survival and growth of APL cells, and to screen potential therapeutic agents that could induce growth arrest through targeting the misfolded N-CoR-induced survival pathways in APL.","abstract_has_math":false,"creators":["NG PING PING ANGELA"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2009,"date_issued":"2009-05-26","date_published":"2009-05-26","updated_at":"2026-07-24T03:33:34Z","subjects":["Unfolded Protein Response, Autophagy, ER stress, Acute Promyelocytic Leukemia, Apoptosis, N-CoR"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":null,"outbound_label":null,"outbound_source":null},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["NG PING PING ANGELA"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.issued","label":"Date","values":["2009-05-26"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://scholarbank.nus.edu.sg/handle/10635/28325"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Unfolded Protein Response, Autophagy, ER stress, Acute Promyelocytic Leukemia, Apoptosis, N-CoR"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://scholarbank.nus.edu.sg/bitstreams/2287db03-ac5b-4618-bc0b-167aa15d6da4/download"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Acute promyelocytic leukemia (APL), a subtype of acute myeloid leukemia (AML), is caused by PML-RARN1, a fusion protein resulting from chromosomal translocation involving the promyelocytic leukemia (PML) and the retinoic acid receptor N1 (RARN1) genes. PML-RARN1 promotes misfolding of nuclear hormone receptor corepressor (N-CoR) and that accumulation of misfolded N-CoR in the ER induces endoplasmic reticulum (ER) stress and activates unfolded protein response (UPR). Although accumulation of misfolded proteins is known to trigger UPR-induced cytotoxic cell death in several neurodegenerative disorders, APL cells are notably resistant to UPR-induced apoptosis. This project was initiated with the goals to investigate how N-CoR misfolding supports the survival and growth of APL cells, and to screen potential therapeutic agents that could induce growth arrest through targeting the misfolded N-CoR-induced survival pathways in APL."]},{"key":"dc:format.checksum.md5","label":"Dc Format Checksum Md5","values":["f918a0399af9691967832d1bd9b9636b","aece9e4afd39a39e349087d7f6cc9d43"]},{"key":"dc:title","label":"Title","values":["Role of Abberant Proteolysis in the Pathogenesis of APL"]}]}],"canonical_facts":{"dc:creator":["NG PING PING ANGELA"],"dc:date.issued":["2009-05-26"],"dc:description.abstract":["Acute promyelocytic leukemia (APL), a subtype of acute myeloid leukemia (AML), is caused by PML-RARN1, a fusion protein resulting from chromosomal translocation involving the promyelocytic leukemia (PML) and the retinoic acid receptor N1 (RARN1) genes. PML-RARN1 promotes misfolding of nuclear hormone receptor corepressor (N-CoR) and that accumulation of misfolded N-CoR in the ER induces endoplasmic reticulum (ER) stress and activates unfolded protein response (UPR). Although accumulation of misfolded proteins is known to trigger UPR-induced cytotoxic cell death in several neurodegenerative disorders, APL cells are notably resistant to UPR-induced apoptosis. This project was initiated with the goals to investigate how N-CoR misfolding supports the survival and growth of APL cells, and to screen potential therapeutic agents that could induce growth arrest through targeting the misfolded N-CoR-induced survival pathways in APL."],"dc:format.checksum.md5":["f918a0399af9691967832d1bd9b9636b","aece9e4afd39a39e349087d7f6cc9d43"],"dc:identifier.uri":["https://scholarbank.nus.edu.sg/bitstreams/2287db03-ac5b-4618-bc0b-167aa15d6da4/download"],"dc:relation.isreferencedby":["https://scholarbank.nus.edu.sg/handle/10635/28325"],"dc:subject":["Unfolded Protein Response, Autophagy, ER stress, Acute Promyelocytic Leukemia, Apoptosis, N-CoR"],"dc:title":["Role of Abberant Proteolysis in the Pathogenesis of APL"],"dc:type":["Thesis"]},"updated_at":"2026-07-24T03:33:34Z"}