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- Publisher Website: 10.1016/j.febslet.2011.07.030
- Scopus: eid_2-s2.0-80052259846
- PMID: 21821031
- WOS: WOS:000294295400017
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Article: Loss of Δnp63α promotes mitotic exit in epithelial cells
Title | Loss of Δnp63α promotes mitotic exit in epithelial cells | ||||||||
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Authors | |||||||||
Keywords | Cell cycle Mitosis p63 | ||||||||
Issue Date | 2011 | ||||||||
Publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febslet | ||||||||
Citation | FEBS Letters, 2011, v. 585 n. 17, p. 2720-2726 How to Cite? | ||||||||
Abstract | Protein p63 is a key regulator in cell proliferation and cell differentiation in stratified squamous epithelium. ΔNp63α is the most commonly expressed p63 isoform, which is often overexpressed in human tumor. In the present work we report the potential involvement of ΔNp63α in cell cycle regulation. ΔNp63α accumulated in mitotic cells but its expression decreased during mitotic exit. Moreover, ΔNp63α knockdown promoted mitotic exit. ΔNp63α shares a conserved destruction box (D-box) motif with other potential targets of the Anaphase-Promoting Complex/Cyclosome (APC/C). Overexpression of APC/C coactivator Cdh1 destabilized ΔNp63α. Our results suggest that ΔNp63α level is cell cycle-regulated and may play a role in the regulation of mitotic exit. © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. | ||||||||
Persistent Identifier | http://hdl.handle.net/10722/137205 | ||||||||
ISSN | 2023 Impact Factor: 3.0 2023 SCImago Journal Rankings: 1.208 | ||||||||
ISI Accession Number ID |
Funding Information: We appreciate the kind gifts from Drs. James DiRenzo (Dartmouth-Hitchcock Medical Center, USA), Kurt Engeland (University of Leipzig, Leipzig, Germany), Patrick Ling (Queensland University of Technology, Australia), Serigo Moreno (University of Salamanca, Spain), Ralph Wasch (Albert-Ludwigs University Medical Center, Freiburg, Germany) and Randy Y.C. Poon (The Hong Kong University of Science and Technology, Hong Kong). This work was supported by Research Grant Council, Hong Kong (HKU7770/07 HKU 7778/09 M), the AoE NPC (AoE/M-06/08) and CRCG grant of University of Hong Kong. | ||||||||
References | |||||||||
Grants |
DC Field | Value | Language |
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dc.contributor.author | Hau, PM | en_HK |
dc.contributor.author | Yip, YL | en_HK |
dc.contributor.author | Huen, MSY | en_HK |
dc.contributor.author | Tsao, SW | en_HK |
dc.date.accessioned | 2011-08-26T14:18:47Z | - |
dc.date.available | 2011-08-26T14:18:47Z | - |
dc.date.issued | 2011 | en_HK |
dc.identifier.citation | FEBS Letters, 2011, v. 585 n. 17, p. 2720-2726 | en_HK |
dc.identifier.issn | 0014-5793 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/137205 | - |
dc.description.abstract | Protein p63 is a key regulator in cell proliferation and cell differentiation in stratified squamous epithelium. ΔNp63α is the most commonly expressed p63 isoform, which is often overexpressed in human tumor. In the present work we report the potential involvement of ΔNp63α in cell cycle regulation. ΔNp63α accumulated in mitotic cells but its expression decreased during mitotic exit. Moreover, ΔNp63α knockdown promoted mitotic exit. ΔNp63α shares a conserved destruction box (D-box) motif with other potential targets of the Anaphase-Promoting Complex/Cyclosome (APC/C). Overexpression of APC/C coactivator Cdh1 destabilized ΔNp63α. Our results suggest that ΔNp63α level is cell cycle-regulated and may play a role in the regulation of mitotic exit. © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. | en_HK |
dc.language | eng | en_US |
dc.publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febslet | en_HK |
dc.relation.ispartof | FEBS Letters | en_HK |
dc.subject | Cell cycle | - |
dc.subject | Mitosis | - |
dc.subject | p63 | - |
dc.subject.mesh | Cell Line, Tumor | en_HK |
dc.subject.mesh | Epithelial Cells - cytology - metabolism | en_HK |
dc.subject.mesh | HeLa Cells | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Immunoblotting | en_HK |
dc.subject.mesh | Mitosis - genetics - physiology | en_HK |
dc.subject.mesh | Protein Isoforms - genetics - metabolism | en_HK |
dc.subject.mesh | RNA, Small Interfering - genetics | en_HK |
dc.subject.mesh | Transcription Factors - genetics - metabolism | en_HK |
dc.subject.mesh | Tumor Suppressor Proteins - genetics - metabolism | en_HK |
dc.title | Loss of Δnp63α promotes mitotic exit in epithelial cells | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Huen, MSY:huen.michael@hku.hk | en_HK |
dc.identifier.email | Tsao, SW:gswtsao@hkucc.hku.hk | en_HK |
dc.identifier.authority | Huen, MSY=rp01336 | en_HK |
dc.identifier.authority | Tsao, SW=rp00399 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.febslet.2011.07.030 | en_HK |
dc.identifier.pmid | 21821031 | - |
dc.identifier.scopus | eid_2-s2.0-80052259846 | en_HK |
dc.identifier.hkuros | 191923 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-80052259846&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 585 | en_HK |
dc.identifier.issue | 17 | en_HK |
dc.identifier.spage | 2720 | en_HK |
dc.identifier.epage | 2726 | en_HK |
dc.identifier.isi | WOS:000294295400017 | - |
dc.publisher.place | Netherlands | en_HK |
dc.relation.project | Centre for Nasopharyngeal Carcinoma Research | - |
dc.identifier.scopusauthorid | Hau, PM=14060079200 | en_HK |
dc.identifier.scopusauthorid | Yip, YL=7005596403 | en_HK |
dc.identifier.scopusauthorid | Huen, MSY=23004751500 | en_HK |
dc.identifier.scopusauthorid | Tsao, SW=7102813116 | en_HK |
dc.identifier.citeulike | 9626325 | - |
dc.identifier.issnl | 0014-5793 | - |