{"id":{"repo_id":"lund","oai_identifier":"oai:lup.lub.lu.se:849623b6-f75d-4602-8b98-d3368b075c72"},"canonical_url":"https://search.dev.ndltd.org/etd/lund/oai:lup.lub.lu.se:849623b6-f75d-4602-8b98-d3368b075c72","repository":{"repo_id":"lund","name":"University of Lund","base_url":"https://lup.lub.lu.se/oai"},"display":{"title":"The role of the leukemia-associated ETO homologue repressors in hematopoiesis","abstract":"The fusion protein AML1-ETO is observed in acute myeloid patients with the chromosomal translocation t(8;21). Cells with this chimeric protein have impaired granulocytic and erythroid differentiation with accumulation of myeloblasts. The transcriptional co-repressor ETO (Eight Twenty One) was identified from the cloning of AML1-ETO. Subsequently, MTGR1 (Myeloid Translocation Gene-Related protein 1) and MTG16 (Myeloid Translocation Gene on chromosome 16) were found to be homologues to ETO, all these proteins being transcriptional co-repressors present in complexes together with other co-repressors such as SIN3, N-CoR and SMRT, and histone deacetylases. The objective of this thesis was to investigate the role of the ETO-homologues in hematopoiesis and leukemia. First, the finding of physical interactions between ETO homologues suggested a possible cooperation. Second, a ubiquitous expression was observed for MTGR1 and MTG16 in hematopoietic lineages. We also discovered that the expression of ETO was restricted to the erythroid lineage suggesting a role for ETO in erythroid development. Furthermore, we found that MTG16 was downregulated during erythroid and granulocytic differentiation, which also implements a role for MTG16 in the regulation of hematopoietic differentiation. Additionally, cells expressing AML1-ETO showed downregulation of MTG16, which possibly can contribute to the impaired differentiation of these cells. Finally, we studied the transcriptional repression of the ETO-homologues in a reporter gene system. MTG16 was found to be a potent co-repressor. Despite a physical interaction, the co-repressors N-CoR and hSIN3B did not augment MTG16-mediated repression. Collectively, our data suggests that the ETO homologues may have differential roles in the regulation of hematopoietic differentiation.","abstract_html":"The fusion protein AML1-ETO is observed in acute myeloid patients with the chromosomal translocation t(8;21). Cells with this chimeric protein have impaired granulocytic and erythroid differentiation with accumulation of myeloblasts. The transcriptional co-repressor ETO (Eight Twenty One) was identified from the cloning of AML1-ETO. Subsequently, MTGR1 (Myeloid Translocation Gene-Related protein 1) and MTG16 (Myeloid Translocation Gene on chromosome 16) were found to be homologues to ETO, all these proteins being transcriptional co-repressors present in complexes together with other co-repressors such as SIN3, N-CoR and SMRT, and histone deacetylases. The objective of this thesis was to investigate the role of the ETO-homologues in hematopoiesis and leukemia. First, the finding of physical interactions between ETO homologues suggested a possible cooperation. Second, a ubiquitous expression was observed for MTGR1 and MTG16 in hematopoietic lineages. We also discovered that the expression of ETO was restricted to the erythroid lineage suggesting a role for ETO in erythroid development. Furthermore, we found that MTG16 was downregulated during erythroid and granulocytic differentiation, which also implements a role for MTG16 in the regulation of hematopoietic differentiation. Additionally, cells expressing AML1-ETO showed downregulation of MTG16, which possibly can contribute to the impaired differentiation of these cells. Finally, we studied the transcriptional repression of the ETO-homologues in a reporter gene system. MTG16 was found to be a potent co-repressor. Despite a physical interaction, the co-repressors N-CoR and hSIN3B did not augment MTG16-mediated repression. Collectively, our data suggests that the ETO homologues may have differential roles in the regulation of hematopoietic differentiation.","abstract_has_math":false,"creators":["Olsson, André"],"institution":"Division of Hematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006","date_published":"2006","updated_at":"2026-07-24T03:00:02Z","subjects":["Hematology","MTGR1","ETO","MTG16","AML1-ETO","hematopoiesis","leukemia","diffferentiation","extracellular fluids","Haematology","Medicin (människa och djur)","extracellulära vätskor","Hematologi","Medicine (human and vertebrates)"],"languages":["eng"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["urn:isbn:91-85559-49-0"],"render_values":[{"text":"urn:isbn:91-85559-49-0","href":null,"code":true}]}]},"links":{"outbound_url":"https://lup.lub.lu.se/record/547372","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Olsson, André"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2006"]},{"key":"dc:publisher","label":"Institution","values":["Division of Hematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University"]},{"key":"dc:type","label":"Dc Type","values":["thesis/doccomp","info:eu-repo/semantics/doctoralThesis","text"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Hematology","MTGR1","ETO","MTG16","AML1-ETO","hematopoiesis","leukemia","diffferentiation","extracellular fluids","Haematology","Medicin (människa och djur)","extracellulära vätskor","Hematologi","Medicine (human and vertebrates)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://lup.lub.lu.se/record/547372","urn:isbn:91-85559-49-0","https://portal.research.lu.se/files/4686653/547373.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The fusion protein AML1-ETO is observed in acute myeloid patients with the chromosomal translocation t(8;21). Cells with this chimeric protein have impaired granulocytic and erythroid differentiation with accumulation of myeloblasts. The transcriptional co-repressor ETO (Eight Twenty One) was identified from the cloning of AML1-ETO. Subsequently, MTGR1 (Myeloid Translocation Gene-Related protein 1) and MTG16 (Myeloid Translocation Gene on chromosome 16) were found to be homologues to ETO, all these proteins being transcriptional co-repressors present in complexes together with other co-repressors such as SIN3, N-CoR and SMRT, and histone deacetylases. The objective of this thesis was to investigate the role of the ETO-homologues in hematopoiesis and leukemia. First, the finding of physical interactions between ETO homologues suggested a possible cooperation. Second, a ubiquitous expression was observed for MTGR1 and MTG16 in hematopoietic lineages. We also discovered that the expression of ETO was restricted to the erythroid lineage suggesting a role for ETO in erythroid development. Furthermore, we found that MTG16 was downregulated during erythroid and granulocytic differentiation, which also implements a role for MTG16 in the regulation of hematopoietic differentiation. Additionally, cells expressing AML1-ETO showed downregulation of MTG16, which possibly can contribute to the impaired differentiation of these cells. Finally, we studied the transcriptional repression of the ETO-homologues in a reporter gene system. MTG16 was found to be a potent co-repressor. Despite a physical interaction, the co-repressors N-CoR and hSIN3B did not augment MTG16-mediated repression. Collectively, our data suggests that the ETO homologues may have differential roles in the regulation of hematopoietic differentiation."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The role of the leukemia-associated ETO homologue repressors in hematopoiesis"]}]}],"canonical_facts":{"dc:creator":["Olsson, André"],"dc:date":["2006"],"dc:description":["The fusion protein AML1-ETO is observed in acute myeloid patients with the chromosomal translocation t(8;21). Cells with this chimeric protein have impaired granulocytic and erythroid differentiation with accumulation of myeloblasts. The transcriptional co-repressor ETO (Eight Twenty One) was identified from the cloning of AML1-ETO. Subsequently, MTGR1 (Myeloid Translocation Gene-Related protein 1) and MTG16 (Myeloid Translocation Gene on chromosome 16) were found to be homologues to ETO, all these proteins being transcriptional co-repressors present in complexes together with other co-repressors such as SIN3, N-CoR and SMRT, and histone deacetylases. The objective of this thesis was to investigate the role of the ETO-homologues in hematopoiesis and leukemia. First, the finding of physical interactions between ETO homologues suggested a possible cooperation. Second, a ubiquitous expression was observed for MTGR1 and MTG16 in hematopoietic lineages. We also discovered that the expression of ETO was restricted to the erythroid lineage suggesting a role for ETO in erythroid development. Furthermore, we found that MTG16 was downregulated during erythroid and granulocytic differentiation, which also implements a role for MTG16 in the regulation of hematopoietic differentiation. Additionally, cells expressing AML1-ETO showed downregulation of MTG16, which possibly can contribute to the impaired differentiation of these cells. Finally, we studied the transcriptional repression of the ETO-homologues in a reporter gene system. MTG16 was found to be a potent co-repressor. Despite a physical interaction, the co-repressors N-CoR and hSIN3B did not augment MTG16-mediated repression. Collectively, our data suggests that the ETO homologues may have differential roles in the regulation of hematopoietic differentiation."],"dc:format":["application/pdf"],"dc:identifier":["https://lup.lub.lu.se/record/547372","urn:isbn:91-85559-49-0","https://portal.research.lu.se/files/4686653/547373.pdf"],"dc:language":["eng"],"dc:publisher":["Division of Hematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:subject":["Hematology","MTGR1","ETO","MTG16","AML1-ETO","hematopoiesis","leukemia","diffferentiation","extracellular fluids","Haematology","Medicin (människa och djur)","extracellulära vätskor","Hematologi","Medicine (human and vertebrates)"],"dc:title":["The role of the leukemia-associated ETO homologue repressors in hematopoiesis"],"dc:type":["thesis/doccomp","info:eu-repo/semantics/doctoralThesis","text"]},"updated_at":"2026-07-24T03:00:02Z"}