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dc.contributor.authorPenas, Clara
dc.contributor.authorGovek, Eve-Ellen
dc.contributor.authorFang, Yin
dc.contributor.authorRamachandran, Vimal
dc.contributor.authorDaniel, Mark
dc.contributor.authorWang, Weiping
dc.contributor.authorMaloof, Marie E
dc.contributor.authorRahaim, Ronald J
dc.contributor.authorBibian, Mathieu
dc.contributor.authorKawauchi, Daisuke
dc.contributor.authorFinkelstein, David
dc.contributor.authorHan, Jeng-Liang
dc.contributor.authorLong, Jun
dc.contributor.authorLi, Bin
dc.contributor.authorRobbins, David J
dc.contributor.authorRoussel, Martine F
dc.contributor.authorRoush, William R
dc.contributor.authorHatten, Mary E
dc.contributor.authorAyad, Nagi G
dc.date.accessioned2020-06-08T16:09:04Z
dc.date.available2020-06-08T16:09:04Z
dc.date.issued2015-04-14
dc.identifier.citationCell Rep . 2015 ;11(2):249-60.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/10289
dc.description.abstractAlthough casein kinase 1δ (CK1δ) is at the center of multiple signaling pathways, its role in the expansion of CNS progenitor cells is unknown. Using mouse cerebellar granule cell progenitors (GCPs) as a model for brain neurogenesis, we demonstrate that the loss of CK1δ or treatment of GCPs with a highly selective small molecule inhibits GCP expansion. In contrast, CK1δ overexpression increases GCP proliferation. Thus, CK1δ appears to regulate GCP neurogenesis. CK1δ is targeted for proteolysis via the anaphase-promoting complex/cyclosome (APC/C(Cdh1)) ubiquitin ligase, and conditional deletion of the APC/C(Cdh1) activator Cdh1 in cerebellar GCPs results in higher levels of CK1δ. APC/C(Cdh1) also downregulates CK1δ during cell-cycle exit. Therefore, we conclude that APC/C(Cdh1) controls CK1δ levels to balance proliferation and cell-cycle exit in the developing CNS. Similar studies in medulloblastoma cells showed that CK1δ holds promise as a therapeutic target.es_ES
dc.description.sponsorshipWe thank Dr. David Rowitch (University of California, San Francisco) for providing the Atoh1-Cre deleter line and Dr. Marc Kirschner for helpful discussions and critical reading of the manuscript. We also thank all members of the Center for Therapeutic Innovation (University of Miami) and the Department of Cancer Biology (Scripps Florida) for helpful suggestions. We thank Dr. Angela MacArthur and the Department of Scientific Editing at St. Jude Children's Research Hospital for helpful suggestions. This work was supported by R21 NS056991 (N.G.A.), R01NS067289 (N.G.A. and M.E.H.), NIH grant NCI CA-096832 (M.F.R.), NIH Molecular Library Screening Center Network grant U54MH074404 (W.R.R., Hugh Rosen, PI), Core Grant CA-021765 (M.F.R., D.K., and D.F.), the Anderson Fellowship (D.K.), and the American Lebanese-Syrian Associated Charities (ALSAC) of St. Jude Children's Research Hospital (M.F.R., D.K., and D.F.) as well as the Spanish Ministerio de Economia y Competitividad (MINECO, SAF2012-38215), Fundacion Ramon Areces, Comunidad de Madrid (S2010/BMD-2470), and the European Union Seventh Framework Programme (MitoSys project; HEALTH-F5-2010-241548) (M.M.).es_ES
dc.language.isoenges_ES
dc.publisherCell Press es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectMITOTIC ENTRYes_ES
dc.subjectUBIQUITINATIONes_ES
dc.subjectMEDULLOBLASTOMAes_ES
dc.subjectD-BOXes_ES
dc.subjectFAMILYes_ES
dc.subjectMOUSE MODELes_ES
dc.subjectSONIC HEDGEHOGes_ES
dc.subjectDEPENDENT DEGRADATIONes_ES
dc.subjectANAPHASE PROMOTING COMPLEXes_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCasein Kinase Idelta es_ES
dc.subject.meshCdh1 Proteins es_ES
dc.subject.meshCell Cycle es_ES
dc.subject.meshCell Proliferation es_ES
dc.subject.meshCentral Nervous System es_ES
dc.subject.meshCerebellum es_ES
dc.subject.meshGene Expression Regulation, Developmental es_ES
dc.subject.meshHeLa Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMice es_ES
dc.subject.meshNeurogenesis es_ES
dc.subject.meshNeurons es_ES
dc.subject.meshRNA Interference es_ES
dc.subject.meshSignal Transduction es_ES
dc.titleCasein kinase 1δ is an APC/C(Cdh1) substrate that regulates cerebellar granule cell neurogenesis.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID25843713es_ES
dc.format.volume11es_ES
dc.format.number2es_ES
dc.format.page249-60es_ES
dc.identifier.doi10.1016/j.celrep.2015.03.016es_ES
dc.contributor.funderUnited States Department of Health and Human Services 
dc.contributor.funderNIH - Molecular Library Screening Center Network
dc.contributor.funderAmerican Lebanese Syrian Associated Charities 
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderUnión Europea 
dc.description.peerreviewedes_ES
dc.identifier.e-issn2211-1247es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.celrep.2015.03.016es_ES
dc.identifier.journalCell reportses_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de División Celular y Cánceres_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/ SAF2012-38215es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/S2010/BMD-2470es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución-NoComercial-CompartirIgual 4.0 Internacional