{"id":{"repo_id":"vcu","oai_identifier":"oai:scholarscompass.vcu.edu:etd-1586"},"canonical_url":"https://search.dev.ndltd.org/etd/vcu/oai:scholarscompass.vcu.edu:etd-1586","repository":{"repo_id":"vcu","name":"Virginia Commonwealth University","base_url":"https://scholarscompass.vcu.edu/do/oai/"},"display":{"title":"The Roles of Krüppel-Like Factor 1 (KLF1) in the Human Fetal Erythroid Compartment.","abstract":"<p>Erythroid Krüppel-like factor (EKLF or KLF1) is a transcription factor with roles in embryonic and adult erythropoiesis. KLF1 knockout mouse embryos die due to severe anemia. Dominant human mutations in KLF1 can cause hereditary persistence of fetal hemoglobin. We show that KLF1 positively regulates β-globin and Bcl11A gene expression using KLF1 knockdown in in vitro-differentiated CD34+ human umbilical cord blood cells. -globin expression appears dependent on KLF1; it is increased with modest KLF1 knockdown but not in cells with low KLF1. KLF2 mRNA amounts are usually increased in KLF1 knockdown. KLF1 knockdown in CD34+ cells results in reduced colony forming ability. Interestingly, the expression of certain proliferation and cell cycle genes is reduced due to KLF1 knockout in mouse or knockdown in human erythroid cells. In conclusion, KLF1 is an important regulator of the β-globin locus and has roles in proliferation and cell cycle.</p>","abstract_html":"&lt;p&gt;Erythroid Krüppel-like factor (EKLF or KLF1) is a transcription factor with roles in embryonic and adult erythropoiesis. KLF1 knockout mouse embryos die due to severe anemia. Dominant human mutations in KLF1 can cause hereditary persistence of fetal hemoglobin. We show that KLF1 positively regulates β-globin and Bcl11A gene expression using KLF1 knockdown in in vitro-differentiated CD34+ human umbilical cord blood cells. -globin expression appears dependent on KLF1; it is increased with modest KLF1 knockdown but not in cells with low KLF1. KLF2 mRNA amounts are usually increased in KLF1 knockdown. KLF1 knockdown in CD34+ cells results in reduced colony forming ability. Interestingly, the expression of certain proliferation and cell cycle genes is reduced due to KLF1 knockout in mouse or knockdown in human erythroid cells. In conclusion, KLF1 is an important regulator of the β-globin locus and has roles in proliferation and cell cycle.&lt;/p&gt;","abstract_has_math":false,"creators":["Mohamad, Safa"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Human Genetics","degree_department":null,"school":null,"contributors":["Joyce Lloyd"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-01-01T08:00:00Z","date_published":"2014-01-01T08:00:00Z","updated_at":"2026-07-24T05:54:02Z","subjects":["KLF1","erythroid","Medical Genetics","Medical Sciences","Medicine and Health Sciences"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/587"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/587","href":"https://scholarscompass.vcu.edu/etd/587","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/C4HT-BK56","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Joyce Lloyd"]},{"key":"dc:creator","label":"Author","values":["Mohamad, Safa"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2019-05-08T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Human Genetics"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["KLF1","erythroid","Medical Genetics","Medical Sciences","Medicine and Health Sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© The Author"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.25772/C4HT-BK56","https://scholarscompass.vcu.edu/etd/587"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p>Erythroid Krüppel-like factor (EKLF or KLF1) is a transcription factor with roles in embryonic and adult erythropoiesis. KLF1 knockout mouse embryos die due to severe anemia. Dominant human mutations in KLF1 can cause hereditary persistence of fetal hemoglobin. We show that KLF1 positively regulates β-globin and Bcl11A gene expression using KLF1 knockdown in in vitro-differentiated CD34+ human umbilical cord blood cells. -globin expression appears dependent on KLF1; it is increased with modest KLF1 knockdown but not in cells with low KLF1. KLF2 mRNA amounts are usually increased in KLF1 knockdown. KLF1 knockdown in CD34+ cells results in reduced colony forming ability. Interestingly, the expression of certain proliferation and cell cycle genes is reduced due to KLF1 knockout in mouse or knockdown in human erythroid cells. In conclusion, KLF1 is an important regulator of the β-globin locus and has roles in proliferation and cell cycle.</p>"]},{"key":"dc:title","label":"Title","values":["The Roles of Krüppel-Like Factor 1 (KLF1) in the Human Fetal Erythroid Compartment."]}]}],"canonical_facts":{"dc:contributor":["Joyce Lloyd"],"dc:creator":["Mohamad, Safa"],"dc:date.available":["2019-05-08T07:00:00Z"],"dc:description.abstract":["<p>Erythroid Krüppel-like factor (EKLF or KLF1) is a transcription factor with roles in embryonic and adult erythropoiesis. KLF1 knockout mouse embryos die due to severe anemia. Dominant human mutations in KLF1 can cause hereditary persistence of fetal hemoglobin. We show that KLF1 positively regulates β-globin and Bcl11A gene expression using KLF1 knockdown in in vitro-differentiated CD34+ human umbilical cord blood cells. -globin expression appears dependent on KLF1; it is increased with modest KLF1 knockdown but not in cells with low KLF1. KLF2 mRNA amounts are usually increased in KLF1 knockdown. KLF1 knockdown in CD34+ cells results in reduced colony forming ability. Interestingly, the expression of certain proliferation and cell cycle genes is reduced due to KLF1 knockout in mouse or knockdown in human erythroid cells. In conclusion, KLF1 is an important regulator of the β-globin locus and has roles in proliferation and cell cycle.</p>"],"dc:identifier":["https://doi.org/10.25772/C4HT-BK56","https://scholarscompass.vcu.edu/etd/587"],"dc:rights":["© The Author"],"dc:subject":["KLF1","erythroid","Medical Genetics","Medical Sciences","Medicine and Health Sciences"],"dc:title":["The Roles of Krüppel-Like Factor 1 (KLF1) in the Human Fetal Erythroid Compartment."],"thesis:degree_discipline":["Human Genetics"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T05:54:02Z"}