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RNA Interference01:23

RNA Interference

RNA interference (RNAi) is a process in which a small non-coding RNA molecule blocks the post-transcriptional expression of a gene by binding to its messenger RNA (mRNA) and preventing the protein from being translated.
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...
RNA Interference01:23

RNA Interference

RNA interference (RNAi) is a process in which a small non-coding RNA molecule blocks the post-transcriptional expression of a gene by binding to its messenger RNA (mRNA) and preventing the protein from being translated.
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...
Experimental RNAi02:15

Experimental RNAi

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...
Leaky Scanning02:28

Leaky Scanning

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 stands for...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Transcriptional Regulation: Riboswitches01:23

Transcriptional Regulation: Riboswitches

Riboswitches are RNA elements that regulate gene expression by altering their secondary structures in response to specific effector molecules. These elements, located in the leader regions of certain mRNAs, act as transcriptional regulators by toggling between alternative conformations to control downstream gene expression. Riboswitch-mediated regulation is a precise mechanism for modulating biosynthetic pathways, as exemplified by the riboflavin biosynthesis pathway in Bacillus...

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Related Experiment Video

Updated: Jun 27, 2026

Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis
09:35

Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis

Published on: August 9, 2013

OLFML3 negatively regulates RIG-I signaling in RNA virus infection.

Qian Gu1, Hong Mei1, Qijun Yu2

  • 1Shanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.

Frontiers in Immunology
|June 26, 2026
PubMed
Summary

Olfactomedin-like protein 3 (OLFML3) suppresses type I interferon signaling during RNA virus infections. This protein interacts with TRIM21, inhibiting RIG-I ubiquitination and destabilizing RIG-I, thus acting as an immunosuppressor.

Keywords:
IFN-I signalingOLFML3RIG-ITRIM21antiviral immunity

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A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
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A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

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Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection
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Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection

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Related Experiment Videos

Last Updated: Jun 27, 2026

Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis
09:35

Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis

Published on: August 9, 2013

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection
06:44

Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection

Published on: January 26, 2019

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Olfactomedin-like protein 3 (OLFML3) is a secreted glycoprotein involved in development and tumorigenesis.
  • Emerging evidence implicates OLFML3 in regulating responses to viral and bacterial infections.
  • This study investigates OLFML3's role in type I interferon (IFN-I) signaling during RNA virus infections.

Purpose of the Study:

  • To elucidate the mechanism by which OLFML3 influences IFN-I signaling in the context of RNA virus infection.
  • To identify OLFML3's interacting partners within the IFN-I signaling pathway.
  • To explore the potential of targeting OLFML3 for antiviral therapeutic strategies.

Main Methods:

  • Quantitative reverse transcription PCR (RT-qPCR) to assess IFN-I production.
  • Olfml3 knockout mice for in vivo infection models.
  • Western blotting and immunofluorescence microscopy to analyze the RIG-I signaling pathway.
  • Mass spectrometry and co-immunoprecipitation (Co-IP) for protein interaction analysis.
  • Gain-of-function and loss-of-function studies for OLFML3 and TRIM21.

Main Results:

  • OLFML3 inhibits IFN-I production by suppressing RIG-I signaling in RNA virus infections.
  • OLFML3 directly interacts with TRIM21, an E3 ubiquitin ligase, via its PRY/SPRY domain.
  • OLFML3 disrupts TRIM21-mediated K63-ubiquitination of RIG-I, leading to RIG-I destabilization and suppressed IFN-I signaling.

Conclusions:

  • OLFML3 acts as a general immunosuppressor in RNA virus infections by inhibiting the RIG-I signaling pathway.
  • Understanding OLFML3's function provides insights into viral immune evasion mechanisms.
  • Targeting OLFML3 may offer a novel therapeutic approach to reactivate IFN-I signaling and combat viral infections.