Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/217146
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dc.contributor.authorPeyman, Mona-
dc.contributor.authorBarroso Fernández, Emma-
dc.contributor.authorTurcu, Andreea L.-
dc.contributor.authorEstrany Jr, Francesc-
dc.contributor.authorSmith, Dáire-
dc.contributor.authorJurado Aguilar, Javier-
dc.contributor.authorRada, Patricia-
dc.contributor.authorMorisseau, Christophe-
dc.contributor.authorHammock, Bruce D.-
dc.contributor.authorValverde, Ángela M.-
dc.contributor.authorPalomer Tarridas, Francesc Xavier-
dc.contributor.authorGaldeano Cantador, Carlos-
dc.contributor.authorVázquez Cruz, Santiago-
dc.contributor.authorVázquez Carrera, Manuel-
dc.date.accessioned2024-12-17T11:58:41Z-
dc.date.available2024-12-17T11:58:41Z-
dc.date.issued2023-10-11-
dc.identifier.issn0753-3322-
dc.identifier.urihttps://hdl.handle.net/2445/217146-
dc.description.abstractSoluble epoxide hydrolase (sEH) is a drug target with the potential for therapeutic utility in the areas of inflammation, neurodegenerative disease, chronic pain, and diabetes, among others. Proteolysis-targeting chimeras (PROTACs) molecules offer new opportunities for targeting sEH, due to its capacity to induce its degradation. Here, we describe that the new ALT-PG2, a PROTAC that degrades sEH protein in the human hepatic Huh-7 cell line, in isolated mouse primary hepatocytes, and in the liver of mice. Remarkably, sEH degradation caused by ALT-PG2 was accompanied by an increase in the phosphorylated levels of AMP-activated protein kinase (AMPK), while phosphorylated extracellular-signal-regulated kinase 1/2 (ERK1/2) was reduced. Consistent with the key role of these kinases on endoplasmic reticulum (ER) stress, ALT-PG2 attenuated the levels of ER stress and inflammatory markers. Overall, the findings of this study indicate that targeting sEH with degraders is a promising pharmacological strategy to promote AMPK activation and to reduce ER stress and inflammation.-
dc.format.extent1 p.-
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherElsevier Masson SAS-
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1016/j.biopha.2023.115667-
dc.relation.ispartofBiomedicine & Pharmacotherapy, 2023, vol. 168, p. 115667-
dc.relation.urihttps://doi.org/10.1016/j.biopha.2023.115667-
dc.rightscc by-nc-nd (c) Mona Peyman, et al., 2023-
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.sourceArticles publicats en revistes (Farmàcia, Tecnologia Farmacèutica i Fisicoquímica)-
dc.subject.classificationEpòxids-
dc.subject.classificationInflamació-
dc.subject.classificationNeurologia-
dc.subject.otherEpoxy compounds-
dc.subject.otherInflammation-
dc.subject.otherNeurology-
dc.titleSoluble epoxide hydrolase-targeting PROTAC activates AMPK and inhibits endoplasmic reticulum stress-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.identifier.idgrec739794-
dc.date.updated2024-12-17T11:58:41Z-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
Appears in Collections:Articles publicats en revistes (Farmàcia, Tecnologia Farmacèutica i Fisicoquímica)
Articles publicats en revistes (Institut de Biomedicina (IBUB))

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