{"id":{"repo_id":"nus","oai_identifier":"oai:scholarbank.nus.edu.sg:10635/15006"},"canonical_url":"https://search.dev.ndltd.org/etd/nus/oai:scholarbank.nus.edu.sg:10635/15006","repository":{"repo_id":"nus","name":"National University of Singapore","base_url":"https://scholarbank.nus.edu.sg/oai/request"},"display":{"title":"Role of c-Jun in the regulation of tumor suppressor p53 homologue, p73","abstract":"This study proposes for the first time that the transcription factor c-Jun stabilizes and activates p73. Genetic evidences consolidated the findings, as c-jun-/- cells are defective in p73 stabilization, transcriptional activation, and are resistant to cisplatin induced apoptosis. Upon introducing c-Jun in c-jun-/- cells restores p73 stabilization, activation, and sensitivity to cisplatin. UV radiation increases p73 levels in a variety of cell lines analyzed. In a parallel study, p73 increases AP-1 activity and it synergies with c-Jun to increase the expression of AP-1 dependent target genes. The NH2-terminus of p73 is necessary to synergizes with c-Jun. JNK-mediated c-Jun phosphorylation is required for its ability to co-operate with p73. Basal level of AP-1 activity was lowered by the dominant negative p73. Further, this study suggests the existence of a regulatory loop between the TA-p73/I?N-p73 and c-Jun. Collectively, this study indicates that c-Jun and p73 regulate each other in cell fate decisions.","abstract_html":"This study proposes for the first time that the transcription factor c-Jun stabilizes and activates p73. Genetic evidences consolidated the findings, as c-jun-/- cells are defective in p73 stabilization, transcriptional activation, and are resistant to cisplatin induced apoptosis. Upon introducing c-Jun in c-jun-/- cells restores p73 stabilization, activation, and sensitivity to cisplatin. UV radiation increases p73 levels in a variety of cell lines analyzed. In a parallel study, p73 increases AP-1 activity and it synergies with c-Jun to increase the expression of AP-1 dependent target genes. The NH2-terminus of p73 is necessary to synergizes with c-Jun. JNK-mediated c-Jun phosphorylation is required for its ability to co-operate with p73. Basal level of AP-1 activity was lowered by the dominant negative p73. Further, this study suggests the existence of a regulatory loop between the TA-p73/I?N-p73 and c-Jun. Collectively, this study indicates that c-Jun and p73 regulate each other in cell fate decisions.","abstract_has_math":false,"creators":["LAKSHMANANE BOOMINATHAN"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2005,"date_issued":"2005-12-02","date_published":"2005-12-02","updated_at":"2026-07-24T03:33:22Z","subjects":["Jun; TA-p73; ΔN-p73 ; Cisplatin; UV"],"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":["LAKSHMANANE BOOMINATHAN"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.issued","label":"Date","values":["2005-12-02"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://scholarbank.nus.edu.sg/handle/10635/15006"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Jun; TA-p73; ΔN-p73 ; Cisplatin; UV"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://scholarbank.nus.edu.sg/bitstreams/9e341f49-2d1d-4942-ac95-9875d0936026/download"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["This study proposes for the first time that the transcription factor c-Jun stabilizes and activates p73. Genetic evidences consolidated the findings, as c-jun-/- cells are defective in p73 stabilization, transcriptional activation, and are resistant to cisplatin induced apoptosis. Upon introducing c-Jun in c-jun-/- cells restores p73 stabilization, activation, and sensitivity to cisplatin. UV radiation increases p73 levels in a variety of cell lines analyzed. In a parallel study, p73 increases AP-1 activity and it synergies with c-Jun to increase the expression of AP-1 dependent target genes. The NH2-terminus of p73 is necessary to synergizes with c-Jun. JNK-mediated c-Jun phosphorylation is required for its ability to co-operate with p73. Basal level of AP-1 activity was lowered by the dominant negative p73. Further, this study suggests the existence of a regulatory loop between the TA-p73/I?N-p73 and c-Jun. 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In a parallel study, p73 increases AP-1 activity and it synergies with c-Jun to increase the expression of AP-1 dependent target genes. The NH2-terminus of p73 is necessary to synergizes with c-Jun. JNK-mediated c-Jun phosphorylation is required for its ability to co-operate with p73. Basal level of AP-1 activity was lowered by the dominant negative p73. Further, this study suggests the existence of a regulatory loop between the TA-p73/I?N-p73 and c-Jun. 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