{"id":{"repo_id":"vcu","oai_identifier":"oai:scholarscompass.vcu.edu:etd-1199"},"canonical_url":"https://search.dev.ndltd.org/etd/vcu/oai:scholarscompass.vcu.edu:etd-1199","repository":{"repo_id":"vcu","name":"Virginia Commonwealth University","base_url":"https://scholarscompass.vcu.edu/do/oai/"},"display":{"title":"Analysis of NFI-X3 and STAT3 Interaction and Its Functions","abstract":"YKL-40 is a secreted protein that is highly up-regulated in malignant glioblastoma (GBM). Its expression is correlated with the invasive nature of GBMs and poor diagnosis of patients (Nigro et al., 2005). Previous research has shown that in astrocytes and GBM cells, YKL-40 expression is regulated by two transcription factors, NFI-X3 and STAT3, which form a complex with each other (Singh et al., 2011). Here, we show that the N-terminal domain of NFI-X3 is sufficient and required for its interaction with STAT3. We also show that the DNA-binding domain of NFI-X3 is required to induce YKL-40 expression. Thus, the interaction of NFI-X3 with STAT3 may play a role in stabilizing the otherwise weak binding of NFI-X3 to the YKL-40 promoter. Collectively, the observations made in this study shed light on the mechanisms by which NFI-X3, in concert with STAT3 regulate YKL-40 expression.","abstract_html":"YKL-40 is a secreted protein that is highly up-regulated in malignant glioblastoma (GBM). Its expression is correlated with the invasive nature of GBMs and poor diagnosis of patients (Nigro et al., 2005). Previous research has shown that in astrocytes and GBM cells, YKL-40 expression is regulated by two transcription factors, NFI-X3 and STAT3, which form a complex with each other (Singh et al., 2011). Here, we show that the N-terminal domain of NFI-X3 is sufficient and required for its interaction with STAT3. We also show that the DNA-binding domain of NFI-X3 is required to induce YKL-40 expression. Thus, the interaction of NFI-X3 with STAT3 may play a role in stabilizing the otherwise weak binding of NFI-X3 to the YKL-40 promoter. Collectively, the observations made in this study shed light on the mechanisms by which NFI-X3, in concert with STAT3 regulate YKL-40 expression.","abstract_has_math":false,"creators":["Tizazu, Etsegenet"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Biochemistry","degree_department":null,"school":null,"contributors":["Kordula Tomasz"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-04T07:00:00Z","date_published":"2011-05-04T07:00:00Z","updated_at":"2026-07-24T05:53:41Z","subjects":["NFI","STAT3","YKL-40","Glioblastoma","Biochemistry, Biophysics, and Structural Biology","Life Sciences"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/200"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/200","href":"https://scholarscompass.vcu.edu/etd/200","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/RGJP-PG52","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Kordula Tomasz"]},{"key":"dc:creator","label":"Author","values":["Tizazu, Etsegenet"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2016-05-11T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biochemistry"]},{"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":["NFI","STAT3","YKL-40","Glioblastoma","Biochemistry, Biophysics, and Structural Biology","Life 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/RGJP-PG52","https://scholarscompass.vcu.edu/etd/200"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["YKL-40 is a secreted protein that is highly up-regulated in malignant glioblastoma (GBM). Its expression is correlated with the invasive nature of GBMs and poor diagnosis of patients (Nigro et al., 2005). Previous research has shown that in astrocytes and GBM cells, YKL-40 expression is regulated by two transcription factors, NFI-X3 and STAT3, which form a complex with each other (Singh et al., 2011). Here, we show that the N-terminal domain of NFI-X3 is sufficient and required for its interaction with STAT3. We also show that the DNA-binding domain of NFI-X3 is required to induce YKL-40 expression. Thus, the interaction of NFI-X3 with STAT3 may play a role in stabilizing the otherwise weak binding of NFI-X3 to the YKL-40 promoter. Collectively, the observations made in this study shed light on the mechanisms by which NFI-X3, in concert with STAT3 regulate YKL-40 expression."]},{"key":"dc:title","label":"Title","values":["Analysis of NFI-X3 and STAT3 Interaction and Its Functions"]}]}],"canonical_facts":{"dc:contributor":["Kordula Tomasz"],"dc:creator":["Tizazu, Etsegenet"],"dc:date.available":["2016-05-11T07:00:00Z"],"dc:description.abstract":["YKL-40 is a secreted protein that is highly up-regulated in malignant glioblastoma (GBM). Its expression is correlated with the invasive nature of GBMs and poor diagnosis of patients (Nigro et al., 2005). Previous research has shown that in astrocytes and GBM cells, YKL-40 expression is regulated by two transcription factors, NFI-X3 and STAT3, which form a complex with each other (Singh et al., 2011). Here, we show that the N-terminal domain of NFI-X3 is sufficient and required for its interaction with STAT3. We also show that the DNA-binding domain of NFI-X3 is required to induce YKL-40 expression. Thus, the interaction of NFI-X3 with STAT3 may play a role in stabilizing the otherwise weak binding of NFI-X3 to the YKL-40 promoter. Collectively, the observations made in this study shed light on the mechanisms by which NFI-X3, in concert with STAT3 regulate YKL-40 expression."],"dc:identifier":["https://doi.org/10.25772/RGJP-PG52","https://scholarscompass.vcu.edu/etd/200"],"dc:rights":["© The Author"],"dc:subject":["NFI","STAT3","YKL-40","Glioblastoma","Biochemistry, Biophysics, and Structural Biology","Life Sciences"],"dc:title":["Analysis of NFI-X3 and STAT3 Interaction and Its Functions"],"thesis:degree_discipline":["Biochemistry"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T05:53:41Z"}