Modifications induced by HIV-1 Tat protein in cellular splicing mechanisms. Homo sapiens

Intracellular Tat101 deregulated the expression of spliceosome core components, such as SF3B2, SF3A1, SFPQ, PCBP1, SYNCRIP, YBX1 and HSP8A/HSP7C, and thus likely the splicing pathway. Viral splicing experiments showed that Tat101 favored the expression of viral unspliced RNA, which are used at the late steps of the viral cycle, rather than spliced RNAs allowing the progression of HIV-1 replication. Overall design: CD4+ T cell line stably transfected with TetOff and pTRE2hyg-Tat72 vectors (Tat72 is the first exon of HIV-1 Tat protein regulator) CD4+ T cell line stably transfected with TetOff and pTRE2hyg-Tat101 vectors (Tat101 contains the first and second exons of HIV-1 Tat protein regulator) CD4+ T cell line stably transfected with TetOff and pTRE2hyg-Tat101C22G vectors (Tat101 contains the first and second exons of HIV-1 Tat protein regulator with the change C22G)