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Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Retroviruses02:33

Retroviruses

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Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
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Related Experiment Video

Updated: May 23, 2025

Identification of Nucleolar Factors During HIV-1 Replication Through Rev Immunoprecipitation and Mass Spectrometry
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BRD9 functions as an HIV-1 latency regulatory factor.

Tsz-Yat Luk1,2, Lok-Yan Yim1,2, Runhong Zhou1,2

  • 1AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region of China.

Proceedings of the National Academy of Sciences of the United States of America
|May 22, 2025
PubMed
Summary

Bromodomain-containing protein 9 (BRD9) inhibition reactivates latent HIV-1 reservoirs, a crucial step for HIV-1 cure. This finding offers a new target for developing effective latency reversal agents to combat HIV.

Keywords:
AIDSBRD9HIV-1 latency

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • HIV-1 cure is hindered by latent viral reservoirs.
  • The "Shock & Kill" strategy aims to reactivate and eliminate these reservoirs.
  • Current latency reversal agents (LRAs) show limited efficacy in fully reactivating latent HIV-1.

Purpose of the Study:

  • To identify novel regulators of HIV-1 latency.
  • To investigate the role of bromodomain-containing protein 9 (BRD9) in HIV-1 latency.

Main Methods:

  • Inhibition, gene depletion, and protein degradation of BRD9.
  • Assays in T cell lines, human resting memory CD4+ T cells, and PBMCs from people living with HIV-1 (PWH) on ART.
  • CUT&RUN DNA sequencing, transcriptomics, and pharmacological analysis.

Main Results:

  • BRD9 inhibition consistently reactivated HIV-1 latency across different cell types.
  • BRD9 inhibition synergized with BRD4 inhibition to enhance HIV-1 production.
  • BRD9 was found to bind the HIV-1 LTR promoter, competing with HIV-1 Tat.
  • Downstream host targets ATAD2 and MTHFD2 were identified as BRD9 modulators of HIV-1 latency.

Conclusions:

  • BRD9 is a novel regulator of HIV-1 latency.
  • Targeting BRD9 represents a promising strategy for HIV-1 cure research.
  • Understanding BRD9's mechanism provides insights into host-pathogen interactions in HIV-1 latency.