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dc.creatorBayoumi, Alies
dc.creatorElsayed, Asmaaes
dc.creatorHan, Shuanglines
dc.creatorPetta, Salvatorees
dc.creatorAdams, Leon A.es
dc.creatorAller, Rocioes
dc.creatorRomero Gómez, Manueles
dc.creatorEslam, Mohammedes
dc.date.accessioned2022-10-26T14:08:50Z
dc.date.available2022-10-26T14:08:50Z
dc.date.issued2021
dc.identifier.issn2198-3844es
dc.identifier.urihttps://hdl.handle.net/11441/138383
dc.description.abstractFibroblast growth factor 21 (FGF21) is a liver-derived hormone with pleiotropic beneficial effects on metabolism. Paradoxically, FGF21 levels are elevated in metabolic diseases. Interventions that restore metabolic homeostasis reduce FGF21. Whether abnormalities in FGF21 secretion or resistance in peripheral tissues is the initiating factor in altering FGF21 levels and function in humans is unknown. A genetic approach is used to help resolve this paradox. The authors demonstrate that the primary event in dysmetabolic phenotypes is the elevation of FGF21 secretion. The latter is regulated by translational reprogramming in a genotype- and context-dependent manner. To relate the findings to tissues outcomes, the minor (A) allele of rs838133 is shown to be associated with increased hepatic inflammation in patients with metabolic associated fatty liver disease. The results here highlight a dominant role for translation of the FGF21 protein to explain variations in blood levels that is at least partially inherited. These results provide a framework for translational reprogramming of FGF21 to treat metabolic diseases.es
dc.formatapplication/pdfes
dc.format.extent16 p.es
dc.language.isoenges
dc.publisherWILEYes
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleMistranslation drives alterations in protein levels and the effects of a synonymous variant at the fibroblast growth factor 21 locuses
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Medicinaes
dc.relation.publisherversionhttps://onlinelibrary.wiley.com/doi/10.1002/advs.202004168es
dc.identifier.doi10.1002/advs.202004168es
dc.contributor.groupUniversidad de Sevilla. CTS 532: Unidad de Hepatologíaes
dc.journaltitleAdvance Sciencees
dc.publication.volumen8es
dc.publication.issue11es
dc.publication.initialPage2004168es

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