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dc.contributor.authorLopez-Huertas, Maria Rosa 
dc.contributor.authorCallejas, S.
dc.contributor.authorAbia, D.
dc.contributor.authorMateos, Elena 
dc.contributor.authorDopazo, A.
dc.contributor.authorAlcamí, José 
dc.contributor.authorCoiras, Mayte
dc.identifier.citationNucleic Acids Res. 2010;38(10):3287-307es_ES
dc.description.abstractThe human immunodeficiency virus type 1 (HIV-1) regulator Tat is essential for viral replication because it achieves complete elongation of viral transcripts. Tat can be released to the extracellular space and taken up by adjacent cells, exerting profound cytoskeleton rearrangements that lead to apoptosis. In contrast, intracellular Tat has been described as protector from apoptosis. Tat gene is composed by two coding exons that yield a protein of 101 amino acids (aa). First exon (1-72aa) is sufficient for viral transcript elongation and second exon (73-101 aa) appears to contribute to non-transcriptional functions. We observed that Jurkat cells stably expressing intracellular Tat101 showed gene expression deregulation 4-fold higher than cells expressing Tat72. Functional experiments were performed to evaluate the effect of this deregulation. First, NF-kappaB-, NF-AT- and Sp1-dependent transcriptional activities were greatly enhanced in Jurkat-Tat101, whereas Tat72 induced milder but efficient activation. Second, cytoskeleton-related functions as cell morphology, proliferation, chemotaxis, polarization and actin polymerization were deeply altered in Jurkat-Tat101, but not in Jurkat-Tat72. Finally, expression of several cell surface receptors was dramatically impaired by intracellular Tat101 but not by Tat72. Consequently, these modifications were greatly dependent on Tat second exon and they could be related to the anergy observed in HIV-1-infected T cells.es_ES
dc.description.sponsorshipPlan Nacional del SIDA (MVI 1434/05–5), FIPSE 36584/06 and 36633/07, VIRHORST Network from Comunidad de Madrid (Spain), FIS PI040614 and PI0808752, ISCIII-RETIC RD06/0006, EUROPRISE Network of Excellence of the EU (Grant no. LSHP CT-2006-037611), and BIO2008-04384 from the Ministerio de Ciencia e Innovación, Espanña. Funding for open access charge: Instituto de Salud Carlos III, Ministry of Science and Technology, Spain.es_ES
dc.publisherOxford University Press es_ES
dc.subject.meshCell Proliferation es_ES
dc.subject.meshChemotaxis es_ES
dc.subject.meshComputational Biology es_ES
dc.subject.meshCytoskeleton es_ES
dc.subject.meshExons es_ES
dc.subject.meshGene Expression es_ES
dc.subject.meshHIV-1 es_ES
dc.subject.meshHumans es_ES
dc.subject.meshJurkat Cells es_ES
dc.subject.meshModels, Moleculares_ES
dc.subject.meshReceptors, Cell Surfacees_ES
dc.subject.meshTranscriptional Activation es_ES
dc.subject.meshtat Gene Products, Human Immunodeficiency Viruses_ES
dc.titleModifications in host cell cytoskeleton structure and function mediated by intracellular HIV-1 Tat protein are greatly dependent on the second coding exones_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.contributor.funderPlan Nacional de Sida (España)
dc.contributor.funderFundación para la Investigación y la Prevención del Sida en España 
dc.contributor.funderGobierno de la Comunidad Autónoma de Madrid
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.identifier.journalNucleic Acids Researches_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/MVI 1434/05–5es_ES
dc.rights.accessRightsopen accesses_ES

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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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