Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/106653
DC FieldValueLanguage
dc.contributor.authorAlmeida, Nuno-
dc.contributor.authorCarrara, Guia-
dc.contributor.authorPalmeira, Carlos M.-
dc.contributor.authorFernandes, Ana S.-
dc.contributor.authorParsons, Maddy-
dc.contributor.authorSmith, Geoffrey L.-
dc.contributor.authorSaraiva, Nuno-
dc.date.accessioned2023-04-14T08:30:07Z-
dc.date.available2023-04-14T08:30:07Z-
dc.date.issued2020-01-
dc.identifier.issn22132317pt
dc.identifier.urihttps://hdl.handle.net/10316/106653-
dc.description.abstractThe mechanisms by which the Golgi apparatus (GA) impacts on cell invasion are poorly understood. The human Golgi Anti-Apoptotic Protein (hGAAP, also known as TMBIM4) is a highly conserved Golgi cation channel that modulates intracellular Ca2+ fluxes. Human GAAP is expressed in all human tissues, is essential for cell viability and provides resistance against a range of apoptotic stresses. Furthermore, hGAAP enhances adhesion and cell migration by increasing the turnover of focal adhesions due to activation of store-operated Ca2+ entry. Here, we describe a GA-derived mechanism that controls cell invasion. The overexpression of hGAAP stimulates 3-dimensional proteolytic cell invasion by a mechanism that is dependent on the accumulation of intracellular hydrogen peroxide, which might be produced by the hGAAP-dependent stimulation of mitochondrial respiration. These findings provide new insight into the complex mechanisms by which Ca2+ and reactive oxygen species signaling contribute to cell invasion and to the role of the GA in these processes.pt
dc.language.isoengpt
dc.publisherElsevierpt
dc.relationUID/DTP/04567/2019pt
dc.relationIsaac Newton grantpt
dc.relationUID/DTP/04567/2016pt
dc.relationSTSM grants from EU-ROS (BM1203) and EuroCellNet (CA15214) COST actionspt
dc.relationGLS is a Wellcome Trust Principal Research Fellow [090315/B/09]pt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subjectCalciumpt
dc.subjectCell invasionpt
dc.subjectGolgi apparatuspt
dc.subjectHydrogen peroxidept
dc.subjectMetabolismpt
dc.subjectTMBIMpt
dc.subject.meshAnimalspt
dc.subject.meshCalcium Signalingpt
dc.subject.meshCell Adhesionpt
dc.subject.meshCell Line, Tumorpt
dc.subject.meshCell Movementpt
dc.subject.meshCell Survivalpt
dc.subject.meshHumanspt
dc.subject.meshHydrogen Peroxidept
dc.subject.meshMCF-7 Cellspt
dc.subject.meshMembrane Proteinspt
dc.subject.meshMicept
dc.subject.meshMitochondriapt
dc.subject.meshNeoplasm Invasivenesspt
dc.subject.meshNeoplasm Transplantationpt
dc.subject.meshNeoplasmspt
dc.subject.meshReactive Oxygen Speciespt
dc.subject.meshUp-Regulationpt
dc.titleStimulation of cell invasion by the Golgi Ion Channel GAAP/TMBIM4 via an H2O2-Dependent Mechanismpt
dc.typearticle-
degois.publication.firstPage101361pt
degois.publication.titleRedox Biologypt
dc.peerreviewedyespt
dc.identifier.doi10.1016/j.redox.2019.101361pt
degois.publication.volume28pt
dc.date.embargo2020-01-01*
uc.date.periodoEmbargo0pt
item.grantfulltextopen-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextCom Texto completo-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitLAETA - Associated Laboratory for Energy, Transports and Aeronautics-
crisitem.author.researchunitADAI - Association for the Development of Industrial Aerodynamics-
crisitem.author.orcid0000-0002-2639-7697-
crisitem.author.orcid0000-0002-7805-002X-
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais
I&D CNC - Artigos em Revistas Internacionais
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