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Acute Loss of Cited2 Impairs Nanog Expression and Decreases Self-Renewal of Mouse Embryonic Stem Cells

2015-03Journal article Open Access
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dc.contributor.authorKranc, Kamil R.
dc.contributor.authorOliveira, Daniel
dc.contributor.authorArmesilla-Diaz, Alejandro
dc.contributor.authorPacheco-Leyva, Ivette
dc.contributor.authorMatias, Ana Catarina
dc.contributor.authorEscapa, Ana Luísa
dc.contributor.authorSubramani, Chithra
dc.contributor.authorWheadon, Helen
dc.contributor.authorTrindade, Marlene
dc.contributor.authorNichols, Jennifer
dc.contributor.authorKaji, Keisuke
dc.contributor.authorEnver, Tariq
dc.contributor.authorBragança, José
dc.date.accessioned2018-12-07T14:53:41Z
dc.date.available2018-12-07T14:53:41Z
dc.date.issued2015-03
dc.description.abstractIdentifying novel players of the pluripotency gene regulatory network centered on Oct4, Sox2, and Nanog as well as delineating the interactions within the complex network is key to understanding self-renewal and early cell fate commitment of embryonic stem cells (ESC). While overexpression of the transcriptional regulator Cited2 sustains ESC pluripotency, its role in ESC functions remains unclear. Here, we show that Cited2 is important for proliferation, survival, and self-renewal of mouse ESC. We position Cited2 within the pluripotency gene regulatory network by defining Nanog, Tbx3, and Klf4 as its direct targets. We also demonstrate that the defects caused by Cited2 depletion are, at least in part, rescued by Nanog constitutive expression. Finally, we demonstrate that Cited2 is required for and enhances reprogramming of mouse embryonic fibroblasts to induced pluripotent stem cells.
dc.description.sponsorshipNational Portuguese through FCT-Fundacao para a Ciencia e a Tecnologia [PEst-OE/EQB/LA0023/2013, PTDC/SAU-ENB/111702/2009]; Camara Municipal de Oeiras; Merck Sharp & Dhome Foundation-Portugal; CRUK; Leukaemia & Lymphoma Research; Kay Kendall Leukaemia Fund; Wellcome Trust; Medical Research Council; Cancer Research UK [12796, 14633]; Great Ormond Street Hospital Childrens Charity [W1062]; Medical Research Council [MC_U137973817, G1000801g, MC_qA137913]
dc.identifier.doi10.1002/stem.1889
dc.identifier.issn1066-5099
dc.identifier.issn1549-4918
dc.identifier.urihttp://hdl.handle.net/10400.1/11640
dc.language.isoeng
dc.peerreviewedyes
dc.publisherWiley
dc.subjectTranscriptional Network
dc.subjectSignaling Pathways
dc.subjectHeart Development
dc.subjectGround-State
dc.subjectPluripotency
dc.subjectCoactivator
dc.subjectGene
dc.subjectHeterogeneity
dc.subjectHif-1-Alpha
dc.subjectDeficiency
dc.titleAcute Loss of Cited2 Impairs Nanog Expression and Decreases Self-Renewal of Mouse Embryonic Stem Cells
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PEst-OE%2FEQB%2FLA0023%2F2013/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-ENB%2F111702%2F2009/PT
oaire.citation.endPage712
oaire.citation.issue3
oaire.citation.startPage699
oaire.citation.titleStem Cells
oaire.citation.volume33
oaire.fundingStream3599-PPCDT
oaire.fundingStream3599-PPCDT
person.familyNameOliveira
person.familyNamePacheco-Leyva
person.familyNameMatias
person.familyNameTrindade
person.familyNameBragança
person.givenNameDaniel
person.givenNameIvette
person.givenNameAna Catarina
person.givenNameMarlene
person.givenNameJosé
person.identifier222659
person.identifier.ciencia-idD414-8513-CFCA
person.identifier.ciencia-idB812-0D5C-4983
person.identifier.ciencia-id701D-019D-0779
person.identifier.ciencia-idAC1D-FA9D-F66F
person.identifier.orcid0000-0003-0622-2934
person.identifier.orcid0000-0003-3006-2264
person.identifier.orcid0000-0002-6385-9117
person.identifier.orcid0000-0001-7072-3392
person.identifier.orcid0000-0001-9566-400X
person.identifier.ridA-9430-2014
person.identifier.scopus-author-id55253361100
person.identifier.scopus-author-id56524572200
person.identifier.scopus-author-id55232110200
person.identifier.scopus-author-id6602220001
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccess
rcaap.typearticle
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