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Related Concept Videos

Cooperative Binding of Transcription Regulators02:13

Cooperative Binding of Transcription Regulators

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Transcriptional regulators bind to specific cis-regulatory sequences in the DNA to regulate gene transcription. These cis-regulatory sequences are very short, usually less than ten nucleotide pairs in length. The short length means that there is a high probability of the exact same sequence randomly occurring throughout the genome.  Since regulators can also bind to groups of similar sequences, this further increases the chances of random binding. Transcriptional regulators form...
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Transcription activators are proteins that promote the transcription of genes from DNA to RNA. In most cases, these proteins contain two separate domains ‒ a domain that binds to DNA and a domain for activating transcription; however, in some cases, a single domain is responsible for both binding and activation of transcription, as seen in the glucocorticoid receptor and MyoD.
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Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells.
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The organization of prokaryotic genes in their genome is notably different from that of eukaryotes. Prokaryotic genes are organized, such that the genes for proteins involved in the same biochemical process or function are located together in groups. This group of genes, along with their regulatory elements, are collectively known as an operon. The functional genes in an operon are transcribed together to give a single strand of mRNA known as polycistronic mRNA.
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Author Spotlight: An Integrated Workflow to Study the Promoter-Centric Spatio-Temporal Genome Architecture in Scarce Cell Populations
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KSHV-encoded vIRF3 Cooperates with Cellular IRF4 to Drive Super-Enhancer Activity through Complex DNA Elements.

Ziyan Liang, Haocong Katherine Ma, Christine B Magdongon

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    |August 20, 2025
    PubMed
    Summary

    Kaposi's sarcoma-associated herpesvirus (KSHV) oncoprotein vIRF3 activates oncogenic super-enhancers (SEs) by binding complex DNA elements with cellular IRF4. This interaction is crucial for primary effusion lymphoma (PEL) cell survival and oncogene activation.

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    Area of Science:

    • Oncology
    • Virology
    • Molecular Biology

    Background:

    • Kaposi's sarcoma-associated herpesvirus (KSHV) oncoprotein vIRF3 is vital for primary effusion lymphoma (PEL) cell survival.
    • vIRF3 collaborates with cellular IRF4 to activate super-enhancers (SEs) that drive oncogenes like MYC and IRF4.

    Purpose of the Study:

    • To identify the specific DNA sequences involved in the vIRF3/IRF4 cooperation.
    • To elucidate the mechanisms by which vIRF3 and IRF4 activate oncogenic SEs in PEL cells.

    Main Methods:

    • Systematic mapping of vIRF3/IRF4-responsive regions within the IRF4-SE.
    • Functional analysis of identified DNA motifs, including AP1 and IRF-related sites.
    • DNA pulldown assays to confirm protein-DNA interactions.

    Main Results:

    • A complex ~83 bp region within the IRF4-SE was identified as critical for vIRF3/IRF4 cooperative activation.
    • vIRF3-mediated activation required an AP1 site, while vIRF3/IRF4 cooperation depended on IRF4 DNA binding and novel IRF-related motifs.
    • These motifs, while necessary, were insufficient alone, suggesting the need for an extended composite element for SE activation.
    • DNA pulldowns confirmed vIRF3 and IRF4 binding to the identified motifs within the IRF4-SE.
    • A similar extended responsive element was found in a PEL MYC-SE.

    Conclusions:

    • vIRF3 activates oncogenic SEs by utilizing complex genetic elements that accommodate unique IRF4 binding configurations.
    • These findings enhance the understanding of vIRF3 and IRF4 roles in KSHV-driven oncogenesis.
    • The study reveals novel mechanisms of SE regulation by viral oncoproteins and host factors.