Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/20687
Title: Intracellular expression of Tat alters mitochondrial functions in T cells: a potential mechanism to understand mitochondrial damage during HIV-1 replication.
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Issue Date: 16-Sep-2015
Citation: Retrovirology.2015 Sep;(12):78
Abstract: HIV-1 replication results in mitochondrial damage that is enhanced during antiretroviral therapy (ART). The onset of HIV-1 replication is regulated by viral protein Tat, a 101-residue protein codified by two exons that elongates viral transcripts. Although the first exon of Tat (aa 1-72) forms itself an active protein, the presence of the second exon (aa 73-101) results in a more competent transcriptional protein with additional functions.
PMID: 26376973
URI: https://hdl.handle.net/20.500.12530/20687
Rights: openAccess
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. U. 12 de Octubre > Artículos

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