RelA-Associated Inhibitor Blocks Transcription of Human Immunodeficiency Virus Type 1 by Inhibiting NF-κB and Sp1 Actions

@article{Takada2002RelAAssociatedIB,
  title={RelA-Associated Inhibitor Blocks Transcription of Human Immunodeficiency Virus Type 1 by Inhibiting NF-$\kappa$B and Sp1 Actions},
  author={Norio Takada and Takaomi Sanda and Hiroshi Okamoto and Jian-ping Yang and Kaori Asamitsu and L Sarol and Genjiro Kimura and Hiroaki Uranishi and Toshifumi Tetsuka and Takashi Okamoto},
  journal={Journal of Virology},
  year={2002},
  volume={76},
  pages={8019 - 8030}
}
ABSTRACT RelA-associated inhibitor (RAI) is an inhibitor of nuclear factor κB (NF-κB) newly identified by yeast two-hybrid screen as an interacting protein of the p65 (RelA) subunit. In this study, we attempted to examine the effect of RAI on transcription and replication of human immunodeficiency virus type 1 (HIV-1). We found that RAI inhibited gene expression from the HIV-1 long terminal repeat (LTR) even at the basal level. Upon in vitro DNA-binding reactions, RAI could directly block the… 
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References

SHOWING 1-10 OF 43 REFERENCES
An interaction between the DNA-binding domains of RelA(p65) and Sp1 mediates human immunodeficiency virus gene activation.
TLDR
It is suggested that the juxtaposition of DNA-binding sites promotes a specific protein interaction between the DNA- binding regions of these transcription factors, required for HIV transcriptional activation and may provide a mechanism to allow for selective activation of kappa B-regulated genes.
Identification of a Novel Inhibitor of Nuclear Factor-κB, RelA-associated Inhibitor*
TLDR
Observations indicate that RAI is another inhibitor of NF-κB in addition to IκB proteins and may confer an alternative mechanism of regulation.
Inhibition of human immunodeficiency virus type 1 replication by a bioavailable serine/threonine kinase inhibitor, fasudil hydrochloride.
TLDR
The findings indicate the feasibility of clinical use of FH and its derivatives in decreasing viral load to prevent clinical development of acquired immunodeficiency syndrome (AIDS) among HIV-1-infected individuals.
Inducible Expression of IκBα Repressor Mutants Interferes with NF-κB Activity and HIV-1 Replication in Jurkat T Cells*
TLDR
Induction of tetracycline-inducible expression of transdominant repressors of IκBα (TD-IκB α) resulted in inhibition of HIV-1 multiplication, as measured by p24 antigen, reverse transcriptase, and viral RNA.
NF-κB subunit p65 binds to 53BP2 and inhibits cell death induced by 53BP2
TLDR
It is reported that 53BP2, a protein previously identified by interaction with wild type p53 and Bcl-2, also binds to p65 in a yeast two-hybrid system and it is found that overexpression of GFP-53BP2 induced apoptosis in transiently transfected cells.
NF-kappa B-mediated chromatin reconfiguration and transcriptional activation of the HIV-1 enhancer in vitro.
TLDR
It is suggested that p50 and Sp1 contribute to the establishment of the nucleosomal arrangement of the uninduced provirus in resting T cells, and that p65 activates transcription by recruitment of the RNA polymerase II transcriptional machinery to the chromatin-repressed basal promoter.
The Promyelocytic Leukemia Protein Interacts with Sp1 and Inhibits Its Transactivation of the Epidermal Growth Factor Receptor Promoter
TLDR
Analysis of the effects of PML on Sp1 DNA binding by electrophoretic mobility shift assay showed that PML could specifically disrupt the binding of Sp1 to DNA, and suggest that the association ofPML and Sp1 represents a novel mechanism for negative regulation of EGFR and other Sp1 target promoters.
Inhibition of Nuclear Factor-κB-mediated Transcription by Association with the Amino-terminal Enhancer of Split, a Groucho-related Protein Lacking WD40 Repeats*
TLDR
Using the yeast two-hybrid system, the protein-protein interaction between AES and the p65 (RelA) subunit of the transcription factor nuclear factor κB (NF-κB), which activates various target genes involved in inflammation, apoptosis, and embryonic development, is identified.
The retinoblastoma gene product RB stimulates Sp1-mediated transcription by liberating Sp1 from a negative regulator.
TLDR
Findings provide evidence for a functional link between two distinct classes of oncoproteins, RB and c-Jun, that are involved in the control of cell growth, and also define a novel mechanism for the regulation of c-jun expression.
Anti-rheumatic compound aurothioglucose inhibits tumor necrosis factor-alpha-induced HIV-1 replication in latently infected OM10.1 and Ach2 cells.
TLDR
Specific staining as well as electron microscopic examinations revealed the accumulation of metal gold in the cells, supporting the previous hypothesis that gold ions could block NF-kappaB-DNA binding by a redox mechanism, indicating that the monovalent gold compound AuTG is a potentially useful drug for the treatment of patients infected with HIV.
...
1
2
3
4
5
...