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dc.creatorGárate-Rascón, M. (María)-
dc.creatorRecalde, M. (Miriam)-
dc.creatorRojo-González, C. (Carla)-
dc.creatorGarcía-Fernández-de-Barrena, M. (Maite)-
dc.creatorAvila, M.A. (Matías Antonio)-
dc.creatorArechederra, M. (María)-
dc.creatorBerasain, C. (Carmen)-
dc.date.accessioned2023-01-17T13:48:03Z-
dc.date.available2023-01-17T13:48:03Z-
dc.date.issued2022-
dc.identifier.citationGárate-Rascón, M. (María); Recalde-Domínguez de Vidaurreta, M. (Miriam); Rojo-González, C. (Carla); et al. "SLU7: a new hub of gene expression regulation-from epigenetics to protein stability in health and disease". International Journal of Molecular Sciences. 23 (21), 2022, 13411es
dc.identifier.issn1422-0067-
dc.identifier.urihttps://hdl.handle.net/10171/64999-
dc.description.abstractSLU7 (Splicing factor synergistic lethal with U5 snRNA 7) was first identified as a splicing factor necessary for the correct selection of 3 ' splice sites, strongly impacting on the diversity of gene transcripts in a cell. More recent studies have uncovered new and non-redundant roles of SLU7 as an integrative hub of different levels of gene expression regulation, including epigenetic DNA remodeling, modulation of transcription and protein stability. Here we review those findings, the multiple factors and mechanisms implicated as well as the cellular functions affected. For instance, SLU7 is essential to secure liver differentiation, genome integrity acting at different levels and a correct cell cycle progression. Accordingly, the aberrant expression of SLU7 could be associated with human diseases including cancer, although strikingly, it is an essential survival factor for cancer cells. Finally, we discuss the implications of SLU7 in pathophysiology, with particular emphasis on the progression of liver disease and its possible role as a therapeutic target in human cancer.-
dc.description.sponsorshipWork in the authors’ laboratories is supported by: CIBERehd; grant PI19/00163 from Insti- tuto de Salud Carlos III (ISCIII) co-financed by “Fondo Europeo de Desarrollo Regional” (FEDER), “Una manera de hacer Europa”; grants PID2019-104265RB-I00/AEI/10.13039/501100011033, from Ministerio de Ciencia, Innovación y Universidades MICINN-Agencia Estatal de Investigación in- tegrado en el Plan Estatal de Investigación Cientifica y Técnica y Innovación, cofinanciado con Fondos FEDER, MCIU/AEI/FEDER; AECC post-doctoral fellowship POSTD18014AREC to M.A.; Ministerio de Educación FPU fellowship FPU18/01461 for M.G.R.; Ministerio de Educación FPI fellowship BES-2017-079883 for M.R.; Ramón y Cajal Program contract RYC2018-024475-1 to M.G.F.B.; Fundación Eugenio Rodríguez Pascual, Fundación Mario Losantos, Fundación M Torres and the generous support of Eduardo Avila.-
dc.language.isoen-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.subjectAlternative splicing-
dc.subjectGene expression-
dc.subjectTranscription-
dc.subjectEpigenetics-
dc.subjectDifferentiation-
dc.subjectStress-
dc.subjectGenomic stability-
dc.subjectCell cycle-
dc.subjectLiver pathophysiology-
dc.subjectCancer-
dc.titleSLU7: a new hub of gene expression regulation-from epigenetics to protein stability in health and disease-
dc.typeinfo:eu-repo/semantics/review-
dc.description.noteThis article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license-
dc.identifier.doi10.3390/ijms232113411-
dadun.citation.number21-
dadun.citation.publicationNameInternational Journal of Molecular Sciences-
dadun.citation.startingPage13411-
dadun.citation.volume23-

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