About: Cep63 Recruits Cdk1 to the Centrosome: Implications for Regulation of Mitotic Entry, Centrosome Amplification, and Genome Maintenance

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About: Cep63 Recruits Cdk1 to the Centrosome: Implications for Regulation of Mitotic Entry, Centrosome Amplification, and Genome Maintenance Goto Sponge NotDistinct Permalink

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
Description	Centrosomes are central regulators of mitosis that are often amplified in cancer cells. Centrosomes function both as organizers of the mitotic spindle and as reaction centers to trigger activation of Cdk1 and G(2)/M transition in the cell cycle, but their functional organization remains incomplete. Recent proteomic studies have identified novel components of the human centrosome including Cep63, a protein of unknown function that Xenopus studies have implicated in mitotic spindle assembly and spindle inactivation after DNA damage. Here, we report that human Cep63 binds to and recruits Cdk1 to centrosomes, and thereby regulates mitotic entry. RNAi-mediated Cep63 depletion in U2OS cancer cells induced polyploidization through mitotic skipping. Elicitation of this phenotype was associated with downregulation of centrosomal Cdk1, mimicking the phenotype induced by direct depletion of Cdk1. In contrast, Cep63 overexpression induced de novo centrosome amplification during cell-cycle interphase. Centrosomes are central regulators of mitosis that are often amplified in cancer cells. Centrosomes function both as organizers of the mitotic spindle and as reaction centers to trigger activation of Cdk1 and G(2)/M transition in the cell cycle, but their functional organization remains incomplete. Recent proteomic studies have identified novel components of the human centrosome including Cep63, a protein of unknown function that Xenopus studies have implicated in mitotic spindle assembly and spindle inactivation after DNA damage. Here, we report that human Cep63 binds to and recruits Cdk1 to centrosomes, and thereby regulates mitotic entry. RNAi-mediated Cep63 depletion in U2OS cancer cells induced polyploidization through mitotic skipping. Elicitation of this phenotype was associated with downregulation of centrosomal Cdk1, mimicking the phenotype induced by direct depletion of Cdk1. In contrast, Cep63 overexpression induced de novo centrosome amplification during cell-cycle interphase. (en)
Title	Cep63 Recruits Cdk1 to the Centrosome: Implications for Regulation of Mitotic Entry, Centrosome Amplification, and Genome Maintenance Cep63 Recruits Cdk1 to the Centrosome: Implications for Regulation of Mitotic Entry, Centrosome Amplification, and Genome Maintenance (en)
skos:prefLabel	Cep63 Recruits Cdk1 to the Centrosome: Implications for Regulation of Mitotic Entry, Centrosome Amplification, and Genome Maintenance Cep63 Recruits Cdk1 to the Centrosome: Implications for Regulation of Mitotic Entry, Centrosome Amplification, and Genome Maintenance (en)
skos:notation	RIV/61989592:15110/11:10225010!RIV12-MSM-15110___
http://linked.open...avai/riv/aktivita	P
http://linked.open...avai/riv/aktivity	P(ED0030/01/01)
http://linked.open...iv/cisloPeriodika	6
http://linked.open...vai/riv/dodaniDat	2012
http://linked.open...aciTvurceVysledku	Bártek, Jiří Mistrík, Martin
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Univerzita Palackého v Olomouci / Lékařská fakulta
http://linked.open...dnocenehoVysledku	189477
http://linked.open...ai/riv/idVysledku	RIV/61989592:15110/11:10225010
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	ABERRATIONS; CDK2-CYCLIN; PROGRESSION; REPLICATION; LOCALIZATION; PHOSPHORYLATION; DUPLICATION; CELLS; AURORA-A; DNA-DAMAGE RESPONSE (en)
http://linked.open.../riv/klicoveSlovo	CELLS LOCALIZATION ABERRATIONS AURORA-A CDK2-CYCLIN DNA-DAMAGE RESPONSE DUPLICATION PHOSPHORYLATION PROGRESSION REPLICATION
http://linked.open...odStatuVydavatele	US - Spojené státy americké
http://linked.open...ontrolniKodProRIV	[33EC1B4E5978]
http://linked.open...i/riv/nazevZdroje	Cancer Research
http://linked.open...in/vavai/riv/obor	FD
http://linked.open...ichTvurcuVysledku	2 (xsd:int)
http://linked.open...cetTvurcuVysledku	10 (xsd:int)
http://linked.open...vavai/riv/projekt	Biomedicine for regional development and human resources
http://linked.open...UplatneniVysledku	2011
http://linked.open...v/svazekPeriodika	71
http://linked.open...iv/tvurceVysledku	Bártek, Jiří Fechter, Anne Hornung, Christin Krämer, Alwin Löffler, Herald Marhold, Joachim Matuszewska, Marc Mistrík, Martin Saffrich, Rainer Westermann, Frank
issn	0008-5472
number of pages	11 (xsd:int)
http://localhost/t...ganizacniJednotka	15110

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