C3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: Involvement in cell death

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dc.contributor.authorGutiérrez Uzquiza, Álvaro
dc.contributor.authorArechederra, María
dc.contributor.authorMolina, Isabel
dc.contributor.authorBaños, Rocío
dc.contributor.authorMaia, Vera
dc.contributor.authorBenito De Las Heras, Manuel R.
dc.contributor.authorGuerrero, Carmen
dc.contributor.authorPorras Gallo, María Almudena
dc.date.accessioned2024-01-17T08:30:25Z
dc.date.available2024-01-17T08:30:25Z
dc.date.issued2010-03
dc.description.abstractWe present here evidences supporting a negative regulation of p38α MAPK activity by C3G in MEFs triggered by stress, which can mediate cell death or survival depending on the stimuli. Upon serum deprivation, C3G induces survival through inhibition of p38α activation, which mediates apoptosis. In contrast, in response to H2O2, C3G behaves as a pro-apoptotic molecule, as its knock-down or knock-out enhances survival through up-regulation of p38α activation, which plays an anti-apoptotic role under these conditions. Moreover, the C3G target, Rap-1, plays an opposite role, also through regulation of p38α MAPK activity. Our data also suggest that changes in the protein levels of some members of the Bcl-2 family could account for the regulation of cell death by C3G and/or Rap-1 through p38α MAPK. Bim/Bcl-xL ratio appears to be important in the regulation of cell survival, both upon serum deprivation and in response to H2O2. In addition, the increase in BNIP-3 levels induced by C3G knock-down in wt cells treated with H2O2 might play a role preventing cell death. Therefore, we can conclude that C3G is a negative regulator of p38α MAPK in MEFs, while Rap-1 is a positive regulator, but both, through the regulation of p38α activity, can promote cell survival or cell death depending on the stimuli.
dc.description.departmentDepto. de Bioquímica y Biología Molecular
dc.description.facultyFac. de Farmacia
dc.description.refereedTRUE
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.sponsorshipMinisterio de Ciencia, Innovación y Universidades (España)
dc.description.sponsorshipComunidad de Madrid
dc.description.sponsorshipUniversidad Complutense de Madrid
dc.description.statuspub
dc.identifier.citationGutiérrez-Uzquiza Á, Arechederra M, Molina I, Baños R, Maia V, Benito M, et al. C3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: Involvement in cell death. Cellular Signalling 2010;22:533–42. https://doi.org/10.1016/j.cellsig.2009.11.008.
dc.identifier.doi10.1016/j.cellsig.2009.11.008
dc.identifier.issn0898-6568
dc.identifier.officialurlhttps://doi.org/10.1016/j.cellsig.2009.11.008
dc.identifier.urihttps://hdl.handle.net/20.500.14352/93512
dc.issue.number3
dc.journal.titleCellular Signalling
dc.language.isoeng
dc.page.final542
dc.page.initial533
dc.publisherElsevier
dc.relation.projectIDinfo:eu-repo/grantAgreement/FIS-PI041131
dc.relation.projectIDinfo:eu-repo/grantAgreement/FIS-PI070071
dc.relation.projectIDinfo:eu-repo/grantAgreement/FISPI041324
dc.relation.projectIDinfo:eu-repo/grantAgreement/FIS-PI070078
dc.relation.projectIDinfo:eu-repo/grantAgreement/CCG07-UCM/SAL-2148
dc.relation.projectIDinfo:eu-repo/grantAgreement/FISPI070078
dc.rights.accessRightsrestricted access
dc.subject.keywordp38 MAPK
dc.subject.keywordC3G
dc.subject.keywordApoptosis
dc.subject.keywordStress
dc.subject.keywordRap-1
dc.subject.ucmBiología molecular (Química)
dc.subject.unesco2302 Bioquímica
dc.titleC3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: Involvement in cell death
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number22
dspace.entity.typePublication
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