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The Implication of mRNA degradation disorders on human dISease: focus on DIS3 and DIS3-Like enzymes

dc.contributor.authorSaramago, Margarida
dc.contributor.authorda Costa, Paulo J.
dc.contributor.authorViegas, Sandra C.
dc.contributor.authorArraiano, Cecília M.
dc.date.accessioned2020-04-30T21:28:05Z
dc.date.available2020-04-30T21:28:05Z
dc.date.issued2019-08-07
dc.descriptionPart of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1157).pt_PT
dc.descriptionL. Romão (ed.), The mRNA Metabolism in Human Disease, Advances in Experimental Medicine and Biology 1157, https://doi.org/10.1007/978-3-030-19966-1_4pt_PT
dc.description.abstractRNA degradation is considered a critical posttranscriptional regulatory checkpoint, maintaining the correct functioning of organisms. When a specific RNA transcript is no longer required in the cell, it is signaled for degradation through a number of highly regulated steps. Ribonucleases (or simply RNases) are key enzymes involved in the control of RNA stability. These enzymes can perform the RNA degradation alone or cooperate with other proteins in RNA degradation complexes. Important findings over the last years have shed light into eukaryotic RNA degradation by members of the RNase II/RNB family of enzymes. DIS3 enzyme belongs to this family and represents one of the catalytic subunits of the multiprotein complex exosome. This RNase has a diverse range of functions, mainly within nuclear RNA metabolism. Humans encode two other DIS3-like enzymes: DIS3L (DIS3L1) and DIS3L2. DIS3L1 also acts in association with the exosome but is strictly cytoplasmic. In contrast, DIS3L2 acts independently of the exosome and shows a distinctive preference for uridylated RNAs. These enzymes have been shown to be involved in important cellular processes, such as mitotic control, and associated with human disorders like cancer. This review shows how the impairment of function of each of these enzymes is implicated in human disease.pt_PT
dc.description.sponsorshipThis work was supported by project LISBOA-01-0145-FEDER-007660 (Microbiologia Molecular, Estrutural e Celular) funded by FEDER funds through COMPETE2020 – Programa Operacional Competitividade e Internacionalização (POCI) and by national funds from FCT (Fundação para a Ciência e a Tecnologia); project PTDC/BIA-MIC/1399/2014 to CMA and project PTDC/BIM-MEC/3749/2014 to SCV. In addition, FCT provides postdoctoral grant ref. SFRH/ BPD/109464/2015 to MS. SCV was financed by program IF of FCT (ref IF/00217/2015).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationAdv Exp Med Biol. 2019;1157:85-98. doi: 10.1007/978-3-030-19966-1_4pt_PT
dc.identifier.doi10.1007/978-3-030-19966-1_4pt_PT
dc.identifier.issn0065-2598
dc.identifier.urihttp://hdl.handle.net/10400.18/6564
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherSpringer Verlagpt_PT
dc.relation.publisherversionhttps://link.springer.com/chapter/10.1007%2F978-3-030-19966-1_4pt_PT
dc.subjectCancerpt_PT
dc.subjectDIS3pt_PT
dc.subjectDIS3L1pt_PT
dc.subjectDIS3L2pt_PT
dc.subjectExoribonucleasept_PT
dc.subjectExosomept_PT
dc.subjectPolyadenylationpt_PT
dc.subjectRNA Degradationpt_PT
dc.subjectRNasept_PT
dc.subjectUridylationpt_PT
dc.subjectDoenças Genéticaspt_PT
dc.subjectGenómica Funcional e Estruturalpt_PT
dc.titleThe Implication of mRNA degradation disorders on human dISease: focus on DIS3 and DIS3-Like enzymespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage98pt_PT
oaire.citation.startPage85pt_PT
oaire.citation.titleAdvances in Experimental Medicine and Biologypt_PT
oaire.citation.volume1157pt_PT
rcaap.embargofctDe acordo com política editorial da revista.pt_PT
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT

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