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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Monitoring Activation of the Antiviral Pattern Recognition Receptors RIG-I And PKR By Limited Protease Digestion and Native PAGE
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Monitoring Activation of the Antiviral Pattern Recognition Receptors RIG-I And PKR By Limited Protease Digestion and Native PAGE

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RACK1 Associates With STING to Promote Type I Interferon Activation and Inhibit Pseudorabies Virus Infection.

Yixuan Li1, Yiyu Liu1, Yu Dai1

  • 1Joint International Research Laboratory of Animal Health and Animal Food Safety, College of Veterinary Medicine, Southwest University, Chongqing, 400715, China, swu.edu.cn.

Transboundary and Emerging Diseases
|December 15, 2025
PubMed
Summary
This summary is machine-generated.

Receptor of activated protein kinase C 1 (RACK1) inhibits Pseudorabies virus (PRV) replication by enhancing Type I Interferon (IFN-I) signaling. RACK1 interacts with STING to promote IFN-I activation and limit PRV infection in swine cells.

Keywords:
RACK1STINGpseudorabies virustype I interferon

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Pseudorabies virus (PRV) causes significant economic losses in global swine production.
  • Receptor of activated protein kinase C 1 (RACK1) is implicated in various viral infections, but its role in PRV is unknown.

Purpose of the Study:

  • To investigate the role of RACK1 in PRV infection and its impact on the host immune response.

Main Methods:

  • PRV infection in porcine kidney-15 (PK-15) cells.
  • Analysis of RACK1, IFN-β, ISG15, and ISG20 expression levels.
  • Investigation of RACK1's interaction with STING and IRF3 phosphorylation.

Main Results:

  • RACK1 expression positively correlated with IFN-β, ISG15, and ISG20 in PRV-infected cells.
  • RACK1 inhibited PRV replication and enhanced Type I Interferon (IFN-I) signaling.
  • RACK1 facilitated STING-dependent IRF3 phosphorylation and interacted with STING, promoting its aggregation.

Conclusions:

  • RACK1 acts as a host factor that limits PRV infection by promoting STING-dependent IFN-I activation.
  • This study enhances understanding of RACK1's antiviral mechanisms and IFN-I responses during PRV infection.