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Article: Loss of Δnp63α promotes mitotic exit in epithelial cells

TitleLoss of Δnp63α promotes mitotic exit in epithelial cells
Authors
Issue Date2011
PublisherElsevier 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?
AbstractProtein 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 Identifierhttp://hdl.handle.net/10722/137205
ISSN
2015 Impact Factor: 3.519
2015 SCImago Journal Rankings: 2.026
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council, Hong KongHKU7770/07 HKU 7778/09 M
AoE NPCAoE/M-06/08
University of Hong Kong
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 FieldValueLanguage
dc.contributor.authorHau, PMen_HK
dc.contributor.authorYip, YLen_HK
dc.contributor.authorHuen, MSYen_HK
dc.contributor.authorTsao, SWen_HK
dc.date.accessioned2011-08-26T14:18:47Z-
dc.date.available2011-08-26T14:18:47Z-
dc.date.issued2011en_HK
dc.identifier.citationFEBS Letters, 2011, v. 585 n. 17, p. 2720-2726en_HK
dc.identifier.issn0014-5793en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137205-
dc.description.abstractProtein 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.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febsleten_HK
dc.relation.ispartofFEBS Lettersen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshEpithelial Cells - cytology - metabolismen_HK
dc.subject.meshHeLa Cellsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoblottingen_HK
dc.subject.meshMitosis - genetics - physiologyen_HK
dc.subject.meshProtein Isoforms - genetics - metabolismen_HK
dc.subject.meshRNA, Small Interfering - geneticsen_HK
dc.subject.meshTranscription Factors - genetics - metabolismen_HK
dc.subject.meshTumor Suppressor Proteins - genetics - metabolismen_HK
dc.titleLoss of Δnp63α promotes mitotic exit in epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailHuen, MSY:huen.michael@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityHuen, MSY=rp01336en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.febslet.2011.07.030en_HK
dc.identifier.pmid21821031-
dc.identifier.scopuseid_2-s2.0-80052259846en_HK
dc.identifier.hkuros191923en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80052259846&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume585en_HK
dc.identifier.issue17en_HK
dc.identifier.spage2720en_HK
dc.identifier.epage2726en_HK
dc.identifier.isiWOS:000294295400017-
dc.publisher.placeNetherlandsen_HK
dc.relation.projectCentre for Nasopharyngeal Carcinoma Research-
dc.identifier.scopusauthoridHau, PM=14060079200en_HK
dc.identifier.scopusauthoridYip, YL=7005596403en_HK
dc.identifier.scopusauthoridHuen, MSY=23004751500en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.citeulike9626325-

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