Cell
MinireviewDoes HIV-1 Tat induce a change in viral initiation rights?
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Cited by (168)
The TAR binding dynamics and its implication in Tat degradation mechanism
2021, Biophysical JournalCitation Excerpt :Thus, many people lived with the potential danger of HIV infection without knowing they were HIV-latent patients. The HIV viral Tat needs to hijack the host positive transcription elongation factor b (P-TEFb) protein and requires cis-acting transactivation response element (TAR) RNA to regulate transcription elongation (3–5). Tat degradation occurs predominantly through the proteasomal pathway.
Post-translational modifications inducing proteasomal degradation to counter HIV-1 infection
2020, Virus ResearchCitation Excerpt :In sum, these reports indicate that SUMOylation of IV-1viral proteins is imperative to modulating HIV-1. The HIV-1 Tat protein enhances the processivity of RNA polymerase II (RNAPII) transcription elongation factor by interacting with the cis-acting transactivation response element (TAR) RNA stem-loop structure (Cullen, 1993; Jones and Peterlin, 1994). In this process, Tat directs the cyclin T/cyclin-dependent kinase 9 (CDK9), P-TEFb subunit to RNAPII through cooperative binding with TAR, which is important for Tat-mediated transactivation of transcription of HIV-1 viral genes (Mancebo et al., 1997; Yang et al., 1997; Zhu et al., 1997).
Development of a dual reporter screening assay for distinguishing the inhibition of HIV Tat-mediated transcription from off-target effects
2017, Journal of Virological MethodsCitation Excerpt :Therefore, other classes of anti-HIV drugs are needed to inhibit this process. HIV transcription involves ordered processes, which are organized by the highly conserved transcription trans-activator (Tat) encoded by the integrated provirus HIV-1 genome (Cullen, 1993). Before Tat expression occurs, low-level basal transcription from the viral promoter is initiated spontaneously by cellular factors, such as nuclear factor κB (Gupta and Good, 1977), Sp1 (Jones et al., 1986), and nuclear factor of activated T cells (Shaw et al., 1988), but the transcript is not elongated efficiently (Laspia et al., 1989).
Dipeptidyl peptidase in autoimmune pathophysiology
2011, Advances in Clinical ChemistryCitation Excerpt :In this regard, a selective decrease in CD26+ T cells has been reported in HIV-1-infected individuals prior to a general decrease in CD4+ T cells [193,194]. Moreover, Tat, a regulatory protein encoded by the HIV-1 genome which has been shown to suppress the response of human peripheral T cells to soluble antigens [195,196], can bind to CD26 and partially inhibit DPPIV enzyme activity [89]. We have shown that the DPPIV enzyme activity of plasma soluble CD26 was low in HIV-1-infected individuals, and was inversely correlated with HIV-1 RNA, and that the in vitro addition of rsCD26 could enhance purified protein derivative-induced lymphocyte proliferation [102].
Inhibition of PKR by RNA and DNA viruses
2006, Virus Research