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Functional Inhibition of Aquaporin-3 With a Gold-Based Compound Induces Blockage of Cell Proliferation

dc.contributor.authorSerna, Ana
dc.contributor.authorGalan-Cobo, Ana
dc.contributor.authorRodrigues, Claudia
dc.contributor.authorSanchez-Gomar, Ismael
dc.contributor.authorToledo-Arahal, Juan Jose
dc.contributor.authorMoura, Teresa
dc.contributor.authorCasini, Angela
dc.contributor.authorSoveral, Graca
dc.contributor.authorEchevarria, Miriam
dc.date.accessioned2025-01-22T13:07:10Z
dc.date.available2025-01-22T13:07:10Z
dc.date.issued2014-03-27
dc.identifier.citationSerna A, Galán-Cobo A, Rodrigues C, Sánchez-Gomar I, Toledo-Aral JJ, Moura TF, Casini A, Soveral G, Echevarría M. Functional inhibition of aquaporin-3 with a gold-based compound induces blockage of cell proliferation. J Cell Physiol. 2014 Nov;229(11):1787-801. doi: 10.1002/jcp.24632. PMID: 24676973.es
dc.identifier.issn0021-9541
dc.identifier.urihttps://hdl.handle.net/20.500.12412/6380
dc.description.abstractThe study investigates the effect of the gold(III) complex Auphen on the proliferation of various mammalian cell lines with different levels of AQP3 expression. Auphen significantly reduced proliferation in cells with high AQP3 expression (A431 and PC12-AQP3) and caused cell cycle arrest in the S-G2/M phases without cytotoxic effects. The antiproliferative effect of Auphen correlates with its ability to inhibit AQP3's glycerol permeability (Pgly), and this effect was confirmed to be dependent on the Cys-40 residue of AQP3. These findings suggest that Auphen could be a targeted therapeutic agent for carcinomas with high AQP3 expression.es
dc.description.abstractEs la versión enviada del artículo. Se puede consultar la versión final en https://doi.org/10.1002/jcp.24632es
dc.language.isoenges
dc.titleFunctional Inhibition of Aquaporin-3 With a Gold-Based Compound Induces Blockage of Cell Proliferationes
dc.typearticlees
dc.identifier.doi10.1002/jcp.24632
dc.issue.number11es
dc.journal.titleJournal of Cellular Physiologyes
dc.page.initial1787es
dc.page.final1801es
dc.rights.accessRightsopenAccesses
dc.volume.number229es


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