Rig-i Activation
Rig-i Activation - Related Videos
12:43
Monitoring Activation of the Antiviral Pattern Recognition Receptors RIG-I And PKR By Limited Protease Digestion and Native PAGE
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Cited by 12 •
2014
Innate defenses to virus infections are triggered by pattern recognition receptors (PRRs). The two cytoplasmic PRRs RIG-I and PKR bind to viral signature RNAs, change conformation, oligomerize, and activate antiviral signaling. Methods are described which allow to conveniently monitor the conformational switching and the oligomerization of these cytoplasmic PRRs.
06:57
Fabrication and Testing of Miniature Automatic Photophoretic Trapping Rigs
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Cited by 2 •
2021
This work describes and characterizes the fabrication of miniature automatic photophoretic trapping rigs.
12:24
Murine Model of CD40-activation of B cells
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Cited by 13 •
2010
In this video, we demonstrate the procedure of CD40-activation and expansion of murine B cells from splenocytes of C57BL/6 mice, which can be used as a model antigen-presenting cell (APC) to study induction of immunity.
13:27
Generation of Human CD40-activated B cells
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Cited by 36 •
2009
In this video we present the ex vivo generation and expansion of human CD40-activated B cells (CD40-B) from peripheral blood mononuclear cells (PBMC) by stimulation with CD40 ligand and interleukin-4.
05:54
An In Vitro Method to Determine the Anti-Apoptotic Activity of Antibodies against TNFα
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2025
This video demonstrates a technique for assessing the efficacy of antibodies against tumor necrosis factor-alpha (TNFα), an inflammatory cytokine, through an in vitro bioanalytical approach. TNFα, when introduced to stressed cells, triggers apoptosis. However, binding to the antibodies confines TNFα, averting apoptosis. The degree of apoptosis is quantified using a bioluminescence assay.
FAQs
The RNA end provides a molecular feature that RIG-I can recognize in the cytosol. Viral RNA bearing an exposed 5′-triphosphate or diphosphate end binds the sensor and promotes its conformational change. This end-dependent recognition helps connect viral RNA detection with a defined antiviral signaling pathway rather than with nonspecific activation by any cytosolic RNA.
The conformational change exposes RIG-I CARD domains, which are signaling regions required for interaction with the MAVS adaptor on mitochondria. This structural transition therefore converts RNA recognition into adaptor engagement. Without this change, detection would not efficiently connect the viral RNA signal to the downstream pathway that induces interferons and inflammatory genes.
MAVS serves as the adaptor that receives the activated RIG-I signal on mitochondria and relays it to TBK1 and IKK complexes. These signaling complexes then stimulate IRF3, IRF7, and NF-κB. The coordinated activity of these transcription factors produces two related outputs: type I interferon expression and induction of inflammatory genes.
The pathway separates downstream transcriptional functions among several activated regulators. IRF3 and IRF7 are linked to type I interferon induction, whereas NF-κB contributes to inflammatory gene expression. Considering these outputs together is important in infection studies because RIG-I activation can be evaluated as a coordinated antiviral and inflammatory response rather than as a single gene response.
A study can follow the sequence from recognition of RNA with exposed 5′-triphosphate or diphosphate ends through the RIG-I conformational change and CARD exposure. It can then examine MAVS engagement, activation of TBK1 and IKK complexes, stimulation of IRF3, IRF7, and NF-κB, and resulting type I interferon or inflammatory gene expression.
RIG-I activation provides a molecular framework for examining how host cells respond to viral infection. The pathway links a viral RNA feature to signaling through MAVS, kinase complexes, and transcription factors, making it useful for interpreting antiviral defense and inflammatory gene induction. This context helps researchers connect molecular sensing with broader host-response studies.
Research on RIG-I activation can identify ways to influence a host pathway that induces type I interferons and inflammatory genes after viral RNA recognition. That knowledge supports investigation of antiviral therapies, vaccine adjuvants, and engineered immune-stimulating treatments. The key research value is linking controlled pathway engagement with desired antiviral or immune-modulating outcomes.