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Host Proteins Ku and HMGA1 As Participants of HIV-1 Transcription.

Shadrina OA, Knyazhanskaya ES, Korolev SP, Gottikh MB - Acta Naturae (2016 Jan-Mar)

Bottom Line: The latency maintenance is also a problematic question.We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1.Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, Leninskie Gory, Moscow, 119991, Russia.

ABSTRACT
Human immunodeficiency virus type 1 is known to use the transcriptional machinery of the host cell for viral gene transcription, and the only viral protein that partakes in this process is Tat, the viral trans-activator of transcription. During acute infection, the binding of Tat to the hairpin at the beginning of the transcribed viral RNA recruits the PTEFb complex, which in turn hyperphosphorylates RNA-polymerase II and stimulates transcription elongation. Along with acute infection, HIV-1 can also lead to latent infection that is characterized by a low level of viral transcription. During the maintenance and reversal of latency, there are no detectable amounts of Tat protein in the cell and the mechanism of transcription activation in the absence of Tat protein remains unclear. The latency maintenance is also a problematic question. It seems evident that cellular proteins with a yet unknown nature or role regulate both transcriptional repression in the latent phase and its activation during transition into the lytic phase. The present review discusses the role of cellular proteins Ku and HMGA1 in the initiation of transcription elongation of the HIV-1 provirus. The review presents data regarding Ku-mediated HIV-1 transcription and its dependence on the promoter structure and the shape of viral DNA. We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1. Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

No MeSH data available.


Related in: MedlinePlus

Putative Ku-binding sites in gene promoters. Ku-binding sites homologous to theNRE-1 sequence in the LTR of the GR strain of MMTV. Direct repeat is shown incolor. Mismatches are denoted by lowercase letters [34].
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Figure 4: Putative Ku-binding sites in gene promoters. Ku-binding sites homologous to theNRE-1 sequence in the LTR of the GR strain of MMTV. Direct repeat is shown incolor. Mismatches are denoted by lowercase letters [34].

Mentions: A sequence whose binding to Ku is considered to be truly sequence-specific andmore preferable compared to Ku binding to DNA ends has been identified in theNRE-1 region (negative regulatory element 1) in the LTR of MMTV retrovirus(Fig. 4)[34]. Theinteraction between Ku and this sequence reduces the efficiency oftranscription from viral LTR. The catalytic subunit DNA-PKcs is believed to beinvolved in this regulation [33, 35].It has been demonstrated that GR(glucocorticoid receptor) [34] and Oct-1[36], the two transcription factorsbinding to 5’-LTR MMTV and activating its transcription, can bein vitro phosphorylated by DNAPK. Specific recruitment ofDNA-PK to the promoter and subsequent phosphorylation of transcription factorsis probably one of the transcriptional regulatory mechanisms.


Host Proteins Ku and HMGA1 As Participants of HIV-1 Transcription.

Shadrina OA, Knyazhanskaya ES, Korolev SP, Gottikh MB - Acta Naturae (2016 Jan-Mar)

Putative Ku-binding sites in gene promoters. Ku-binding sites homologous to theNRE-1 sequence in the LTR of the GR strain of MMTV. Direct repeat is shown incolor. Mismatches are denoted by lowercase letters [34].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4837570&req=5

Figure 4: Putative Ku-binding sites in gene promoters. Ku-binding sites homologous to theNRE-1 sequence in the LTR of the GR strain of MMTV. Direct repeat is shown incolor. Mismatches are denoted by lowercase letters [34].
Mentions: A sequence whose binding to Ku is considered to be truly sequence-specific andmore preferable compared to Ku binding to DNA ends has been identified in theNRE-1 region (negative regulatory element 1) in the LTR of MMTV retrovirus(Fig. 4)[34]. Theinteraction between Ku and this sequence reduces the efficiency oftranscription from viral LTR. The catalytic subunit DNA-PKcs is believed to beinvolved in this regulation [33, 35].It has been demonstrated that GR(glucocorticoid receptor) [34] and Oct-1[36], the two transcription factorsbinding to 5’-LTR MMTV and activating its transcription, can bein vitro phosphorylated by DNAPK. Specific recruitment ofDNA-PK to the promoter and subsequent phosphorylation of transcription factorsis probably one of the transcriptional regulatory mechanisms.

Bottom Line: The latency maintenance is also a problematic question.We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1.Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, Leninskie Gory, Moscow, 119991, Russia.

ABSTRACT
Human immunodeficiency virus type 1 is known to use the transcriptional machinery of the host cell for viral gene transcription, and the only viral protein that partakes in this process is Tat, the viral trans-activator of transcription. During acute infection, the binding of Tat to the hairpin at the beginning of the transcribed viral RNA recruits the PTEFb complex, which in turn hyperphosphorylates RNA-polymerase II and stimulates transcription elongation. Along with acute infection, HIV-1 can also lead to latent infection that is characterized by a low level of viral transcription. During the maintenance and reversal of latency, there are no detectable amounts of Tat protein in the cell and the mechanism of transcription activation in the absence of Tat protein remains unclear. The latency maintenance is also a problematic question. It seems evident that cellular proteins with a yet unknown nature or role regulate both transcriptional repression in the latent phase and its activation during transition into the lytic phase. The present review discusses the role of cellular proteins Ku and HMGA1 in the initiation of transcription elongation of the HIV-1 provirus. The review presents data regarding Ku-mediated HIV-1 transcription and its dependence on the promoter structure and the shape of viral DNA. We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1. Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

No MeSH data available.


Related in: MedlinePlus