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dc.contributor.authorRojas-Rivera, Diego [Univ Mayor, Fac Sci, Ctr Integrat Biol]es_CL
dc.contributor.authorDondelinger, Yves; Delanghe, Tom; Priem, Dario; Wynosky-Dolfi, Meghan A.; Sorobetea, Daniel; Giansanti, Piero; Roelandt, Ria; Gropengiesser, Julia; Ruckdeschel, Klaus; Savvides, Savvas N.; Heck, Albert J. R.; Vandenabeele, Peter; Brodsky, Igor E.; Bertrand, Mathieu J. M.es_CL
dc.date.accessioned2020-04-12T14:11:55Z
dc.date.accessioned2020-04-14T15:28:50Z
dc.date.available2020-04-12T14:11:55Z
dc.date.available2020-04-14T15:28:50Z
dc.date.issued2019es_CL
dc.identifier.citationDondelinger, Y., Delanghe, T., Priem, D., Wynosky-Dolfi, M. A., Sorobetea, D., Rojas-Rivera, D., ... & Savvides, S. N. (2019). Serine 25 phosphorylation inhibits RIPK1 kinase-dependent cell death in models of infection and inflammation. Nature communications, 10(1), 1-16.es_CL
dc.identifier.issn2041-1723es_CL
dc.identifier.urihttps://doi.org/10.1038/s41467-019-09690-0es_CL
dc.identifier.urihttp://repositorio.umayor.cl/xmlui/handle/sibum/6325
dc.description.abstractRIPK1 regulates cell death and inflammation through kinase-dependent and -independent mechanisms. As a scaffold, RIPK1 inhibits caspase-8-dependent apoptosis and RIPK3/MLKL-dependent necroptosis. As a kinase, RIPK1 paradoxically induces these cell death modalities. The molecular switch between RIPK1 pro-survival and pro-death functions remains poorly understood. We identify phosphorylation of RIPK1 on Ser25 by IKKs as a key mechanism directly inhibiting RIPK1 kinase activity and preventing TNF-mediated RIPK1-dependent cell death. Mimicking Ser25 phosphorylation (S > D mutation) protects cells and mice from the cytotoxic effect of TNF in conditions of IKK inhibition. In line with their roles in IKK activation, TNF-induced Ser25 phosphorylation of RIPK1 is defective in TAK1- or SHARPIN-deficient cells and restoring phosphorylation protects these cells from TNF-induced death. Importantly, mimicking Ser25 phosphorylation compromises the in vivo cell death-dependent immune control of Yersinia infection, a physiological model of TAK1/IKK inhibition, and rescues the cell death-induced multi-organ inflammatory phenotype of the SHARPIN-deficient mice.es_CL
dc.description.sponsorshipVlaams Instituut voor Bio-technologie (VIB)(Tech Watch); Ghent UniversityGhent University; Fonds voor Wetenschappelijk Onderzoek Vlaanderen (FWO)FWO [G013715N, G044518N, EOS MODEL-IDI 30826052]; Belgian science policy office (BELSPO)Belgian Federal Science Policy Office [IAP 7/32]; Flemish Government [Methusalem BOF09/01M00709, BOF16/MET_V/007]; FWOFWO [G013715N]; Netherlands Organization for Scientific Research (NWO) through the large-scale proteomics facility Proteins@Work [184.032.201]; Deutsche ForschungsgemeinschaftGerman Research Foundation (DFG)es_CL
dc.description.sponsorshipWe are grateful to K. Lemeire (VIB-UGent, Belgium), T. Divert (VIB-UGent, Belgium), B. Gilbert (VIB-UGent, Belgium) and S. Men Choi (VIB-UGent, Belgium) for technical assistance. We would like to thank Prof. A. Degterev (Tufts University, USA) and Dr. R. Merceron (VIB-UGent, Belgium) for scientific advices. We also thank Prof. H. Walczak (UCL, UK) for the Shpn<SUP>cpdm</SUP> mice, Dr. J. Bertin (GSK, USA) for the Ripk1<SUP>K45A</SUP> mice, Prof. J. Silke (WEHI, Australia) for the Shpn<SUP>cpdm</SUP> MDFs and Prof. E. Dejardin (GIGA, Belgium) for the Ikk alpha/ss<SUP>-/-</SUP> MEFs. Research in the group of Prof. M.J.M. Bertrand is financially supported by the Vlaams Instituut voor Bio-technologie (VIB)(Tech Watch co-funding), by the Ghent University, by grants from the Fonds voor Wetenschappelijk Onderzoek Vlaanderen (FWO)(G013715N, G044518N, EOS MODEL-IDI 30826052), from the Belgian science policy office (BELSPO)(IAP 7/32) and from the Flemish Government-accorded to Prof. P. Vandenabeele (Methusalem BOF09/01M00709 and BOF16/MET_V/007). Dr. Y. Dondelinger is supported by a postdoctoral fellowship from the FWO. T. Delanghe and D. Priem have a strategic basic research PhD fellowship from the FWO. Dr. D. Rojas-Rivera. was paid by FWO grant G013715N. The proteomics research in the group of Prof. A. Heck was financially supported by the Netherlands Organization for Scientific Research (NWO) through funding of the large-scale proteomics facility Proteins@Work (project 184.032.201) embedded in the Netherlands Proteomics Centre. Prof. K. Ruckdeschel obtained funding by the Deutsche Forschungsgemeinschaft.es_CL
dc.language.isoenes_CL
dc.publisherNATURE PUBLISHING GROUPes_CL
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceNat. Commun., ABR, 2019. 10
dc.subjectMultidisciplinary Scienceses_CL
dc.titleSerine 25 phosphorylation inhibits RIPK1 kinase-dependent cell death in models of infection and inflammationes_CL
dc.typeArtículoes_CL
umayor.facultadCIENCIAS
umayor.politicas.sherpa/romeoDOAJ Gold, Green Publishedes_CL
umayor.indexadoWOS:000464494000003es_CL
umayor.indexadoPMID: 30988283es_CL
dc.identifier.doiDOI: 10.1038/s41467-019-09690-0es_CL]
umayor.indicadores.wos-(cuartil)Q1es_CL
umayor.indicadores.scopus-(scimago-sjr)SCIMAGO/ INDICE H: 248 Hes_CL


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