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dc.contributor.authorValenzuela Fernández, Agustín 
dc.contributor.authorCabrera Rodríguez, Romina 
dc.contributor.authorPérez Yanes, Silvia
dc.contributor.authorMontelongo, Rafaela
dc.contributor.authorLorenzo Salazar, José M.
dc.contributor.authorEstévez Herrera, Judith
dc.contributor.authorGarcía Luis, Jonay
dc.contributor.authorÍñigo Campos, Antonio
dc.contributor.authorRubio Rodríguez, Luis A.
dc.contributor.authorMuñoz Barrera, Adrián
dc.contributor.authorTrujillo González, Rodrigo Francisco 
dc.contributor.authorDorta Guerra, Roberto 
dc.contributor.authorCasado, Concha
dc.contributor.authorPernas, María
dc.contributor.authorBlanco, Julià
dc.contributor.authorFlores, Carlos
dc.contributor.otherMedicina Física y Farmacología
dc.contributor.otherGrupo "Inmunología Celular y Viral"
dc.date.accessioned2024-01-15T21:10:24Z
dc.date.available2024-01-15T21:10:24Z
dc.date.issued2022
dc.identifier.urihttp://riull.ull.es/xmlui/handle/915/35372
dc.description.abstractThe transactive response DNA-binding protein (TARDBP/TDP-43) influences the processing of diverse transcripts, including that of histone deacetylase 6 (HDAC6). Here, we assessed TDP-43 activity in terms of regulating CD4+ T-cell permissivity to HIV-1 infection. We observed that overexpression of wt-TDP-43 increased both mRNA and protein levels of HDAC6, resulting in impaired HIV-1 infection independently of the viral envelope glycoprotein complex (Env) tropism. Consistently, using an HIV-1 Env-mediated cell-to-cell fusion model, the overexpression of TDP-43 levels negatively affected viral Env fusion capacity. Silencing of endogenous TDP-43 significantly decreased HDAC6 levels and increased the fusogenic and infection activities of the HIV-1 Env. Using pseudovirus bearing primary viral Envs from HIV-1 individuals, overexpression of wt-TDP-43 strongly reduced the infection activity of Envs from viremic non-progressors (VNP) and rapid progressors (RP) patients down to the levels of the inefficient HIV-1 Envs observed in long-term non-progressor elite controllers (LTNP-EC). On the contrary, silencing endogenous TDP-43 significantly favored the infectivity of primary Envs from VNP and RP individuals, and notably increased the infection of those from LTNP-EC. Taken together, our results indicate that TDP-43 shapes cell permissivity to HIV-1 infection, affecting viral Env fusion and infection capacities by altering the HDAC6 levels and associated tubulin-deacetylase anti-HIV-1 activityen
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.relation.ispartofseriesInternational Journal of Molecular Science, 2022, 23, 6180.
dc.rightsLicencia Creative Commons (Reconocimiento-No comercial-Sin obras derivadas 4.0 Internacional)
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es_ES
dc.titleTransactive Response DNA- Binding Protein (TARDBP/TDP-43) Regulates Cell Permissivity to HIV- 1 Infection by Acting on HDAC6.en
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.3390/ijms23116180
dc.subject.keywordTARDBP/TDP-43en
dc.subject.keywordHDAC6en
dc.subject.keywordpore fusion formationen
dc.subject.keywordcell-permissivityen
dc.subject.keywordHIV-1 infectionen


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