Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/178662
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dc.contributor.authorJurado, Manuel-
dc.contributor.authorCastaño Linares, Óscar-
dc.contributor.authorZorzano Olarte, Antonio-
dc.date.accessioned2021-06-23T11:04:36Z-
dc.date.available2021-06-23T11:04:36Z-
dc.date.issued2021-04-20-
dc.identifier.urihttp://hdl.handle.net/2445/178662-
dc.description.abstractThe extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) pathway involves a three-step cascade of kinases that transduce signals and promote processes such as cell growth, development, and apoptosis. An aberrant response of this pathway is related to the proliferation of cell diseases and tumors. By using simulation modeling, we document that the protein arginine methyltransferase 5 (PRMT5) modulates the MAPK pathway and thus avoids an aberrant behavior. PRMT5 methylates the Raf kinase, reducing its catalytic activity and thereby, reducing the activation of ERK in time and amplitude. Two minimal computational models of the epidermal growth factor (EGF)-Ras-ERK MAPK pathway influenced by PRMT5 were proposed: a first model in which PRMT5 is activated by EGF and a second one in which PRMT5 is stimulated by the cascade response. The reported results show that PRMT5 reduces the time duration and the expression of the activated ERK in both cases, but only in the first model PRMT5 limits the EGF range that generates an ERK activation. Based on our data, we propose the protein PRMT5 as a regulatory factor to develop strategies to fight against an excessive activity of the MAPK pathway, which could be of use in chronic diseases and cancer.ca
dc.format.extent12 p.-
dc.format.mimetypeapplication/pdf-
dc.language.isoengca
dc.publisherPergamonca
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1016/j.compbiomed.2021.104339-
dc.relation.ispartofComputers in Biology and Medicine, 2021, vol. 133, p. 104339-
dc.relation.urihttps://doi.org/10.1016/j.compbiomed.2021.104339-
dc.rightscc by (c) Jurado, Manuel et al., 2021-
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subject.classificationProteïnes quinases-
dc.subject.classificationApoptosi-
dc.subject.classificationCàncer-
dc.subject.otherProtein kinases-
dc.subject.otherApoptosis-
dc.subject.otherCancer-
dc.titleStochastic modulation evidences a transitory EGF-Ras-ERK MAPK activity induced by PRMT5ca
dc.typeinfo:eu-repo/semantics/articleca
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.identifier.idgrec713650-
dc.date.updated2021-06-01T07:57:31Z-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca
dc.identifier.idimarina6517002-
dc.identifier.idimarina6518351-
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona))
Articles publicats en revistes (Enginyeria Electrònica i Biomèdica)
Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC))
Articles publicats en revistes (Institut de Nanociència i Nanotecnologia (IN2UB))

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