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dc.contributor.authorMonsalve, Francisco A.
dc.contributor.authorRojas, Armando
dc.contributor.authorGonzalez, Ileana
dc.contributor.authorPerez, Ramón
dc.contributor.authorAñasco, Carolina
dc.contributor.authorRomero, Jacqueline
dc.contributor.authorAraya, Paulina
dc.contributor.authorSantos, Leonardo S.
dc.contributor.authorDelgado-López, Fernando
dc.date.accessioned2023-05-10T16:56:28Z
dc.date.available2023-05-10T16:56:28Z
dc.date.issued2020
dc.identifier.urihttp://repositorio.ucm.cl/handle/ucm/4775
dc.description.abstractReceptor internalization and degradation (RID), is a transmembrane protein coded within the E3 region expression cassette of adenoviruses. RID downregulates the cell surface expression of epidermal growth factor receptor (EGFR), tumor necrosis factor receptor (TNFR), and apoptosis antigen 1 (FAS), causing a reduction of the effects of their respective ligands. In addition, RID inhibits apoptosis by decreasing the secretion of TNF-related apoptosis-inducing ligand (TRAIL) by normal tissue cells. In this article, we report that RID inhibited chemokine expression in human breast cancer cell line MDA-MB-231 but showed no effect in cell line MCF7. These dissimilar results may be due to the different molecular and functional properties of both cell lines. Therefore, it is necessary to replicate this study in other breast cancer cell models.es_CL
dc.language.isoenes_CL
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
dc.sourceMediators of Inflammation, 2020, 2707635es_CL
dc.titleRID: evaluation of the possible inhibiting effect of the proinflammatory signaling induced by TNF-α through NF-κβ and AP-1 in two cell lines of breast canceres_CL
dc.typeArticlees_CL
dc.ucm.indexacionScopuses_CL
dc.ucm.indexacionIsies_CL
dc.ucm.uriwww.hindawi.com/journals/mi/2020/2707635/es_CL
dc.ucm.doidoi.org/10.1155/2020/2707635es_CL


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Atribución-NoComercial-SinDerivadas 3.0 Chile
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