Logo do repositório
 
Publicação

The Role of Cerl2 in the Establishment of Left-Right Asymmetries during Axis Formation and Heart Development

2017-12-10Recensão Acesso aberto
Ver registo simples
dc.contributor.authorBelo, José A
dc.contributor.authorA. Belo, José
dc.contributor.authorMarques, Sara
dc.contributor.authorInácio, José M
dc.contributor.institutionCentro de Estudos de Doenças Crónicas (CEDOC)
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pble-Century Publishing
dc.date.accessioned2018-06-30T02:08:58Z
dc.date.available2018-06-30T02:08:58Z
dc.date.issued2017-12-10
dc.descriptionThis work was supported by Fundação para a Ciência e a Tecnologia (PTDC/BIM-MED/3363/2014). iNOVA4Health—UID/Multi/04462/2013, a program financially supported by Fundação para a Ciência e Tecnologia/Ministério da Educação e Ciência, through national funds and co-funded by FEDER under the PT2020 Partnership Agreement is acknowledged.
dc.description.abstractThe formation of the asymmetric left-right (LR) body axis is one of the fundamental aspects of vertebrate embryonic development, and one still raising passionate discussions among scientists. Although the conserved role of nodal is unquestionable in this process, several of the details around this signaling cascade are still unanswered. To further understand this mechanism, we have been studying Cerberus-like 2 (Cerl2), an inhibitor of Nodal, and its role in the generation of asymmetries in the early vertebrate embryo. The absence of Cerl2 results in a wide spectrum of malformations commonly known as heterotaxia, which comprises defects in either global organ position (e.g., situs inversus totalis), reversed orientation of at least one organ (e.g., situs ambiguus), and mirror images of usually asymmetric paired organs (e.g., left or right isomerisms of the lungs). Moreover, these laterality defects are frequently associated with congenital heart diseases (e.g., transposition of the great arteries, or atrioventricular septal defects). Here, reviewing the knowledge on the establishment of LR asymmetry in mouse embryos, the emerging conclusion is that as necessary as is the activation of the Nodal signaling cascade, the tight control that Cerl2-mediates on Nodal signaling is equally important, and that generates a further regionalized LR genetic program in the proper time and space.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent2315424
dc.identifier.doi10.3390/jcdd4040023
dc.identifier.issn2160-200X
dc.identifier.otherPURE: 4551661
dc.identifier.otherPURE UUID: 80ca4108-8ca7-4fc4-a6bb-7b9b2ba0b2ce
dc.identifier.otherPubMed: 29367552
dc.identifier.otherPubMedCentral: PMC5753124
dc.identifier.otherScopus: 85046768091
dc.identifier.urihttp://hdl.handle.net/10362/40540
dc.language.isoeng
dc.peerreviewedyes
dc.relationinfo:eu-repo/grantAgreement/FCT/5876/147260/PT
dc.subjectCerl2
dc.subjectLR-asymmetry
dc.subjectNodal signaling;
dc.subjectongenital heart diseases
dc.titleThe Role of Cerl2 in the Establishment of Left-Right Asymmetries during Axis Formation and Heart Developmenten
dc.typereview
degois.publication.issue4
degois.publication.titleAmerican journal of cardiovascular disease
degois.publication.volume4
dspace.entity.typePublication
oaire.awardNumberUID/Multi/04462/2013
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FMulti%2F04462%2F2013/PT
oaire.fundingStream5876
person.familyNameBelo
person.givenNameJosé A.
person.identifier.ciencia-idBF13-08E9-25E6
person.identifier.orcid0000-0001-7384-0949
person.identifier.ridF-4444-2012
person.identifier.scopus-author-id6602141392
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccess
relation.isAuthorOfPublication9f75224c-9cf2-478f-9c7c-d22527950642
relation.isAuthorOfPublication.latestForDiscovery9f75224c-9cf2-478f-9c7c-d22527950642
relation.isProjectOfPublication828e3044-8984-4282-bc90-98654cc2323e
relation.isProjectOfPublication.latestForDiscovery828e3044-8984-4282-bc90-98654cc2323e

Ficheiros

Coleções

NMS: CEDOC - Artigos em revista internacional com arbitragem científica