mProX™ Human RIGI Stable Cell Line
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- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 Expression plasmids for FLAG-PD-L1 and HA-RIGI were introduced into HEK293T cells, and the interaction between these two proteins was subsequently confirmed upon their ectopic expression.
The interaction between endogenous and exogenous PD-L1 and RIG-I was analyzed using Co-IP in CT26 and HEK293T cells.
Ref: Zhang, Yangyang, et al. "RIG-I promotes immune evasion of colon cancer by modulating PD-L1 ubiquitination." Journal for Immunotherapy of Cancer 11.9 (2023).
Pubmed: 37758653
DOI: 10.1136/jitc-2023-007313
Research Highlights
Mueller, Martin, et al. "ORF3c is expressed in SARS-CoV-2 infected cells and suppresses immune activation by inhibiting innate sensing." bioRxiv (2023): 2023-02.
In this study, it was found that certain proteins of SARS-CoV-2 are translated from subgenomic RNAs, with the ORF3a sgRNA coding for not just ORF3a, but also for the enigmatic ORF3c, a 41-amino-acid peptide. The expression of ORF3c was observed in cells infected with SARS-CoV-2, and it was found to inhibit RIG-I and MDA5-mediated IFN-β induction. It was also discovered that ORF3c interacts with the signaling adaptor MAVS and hinders the interaction of RIG-I with MAVS. This immunosuppressive activity was found to be present in other sarbecoviruses, including SARS-CoV. However, the delta and kappa variants of SARS-CoV-2 were detected with premature stop codons in ORF3c, suggesting that this reading frame is not essential for viral replication and may be compensated by other proteins. Moreover, disrupting ORF3c did not have a significant effect on SARS-CoV-2 replication in different cell types. This study highlights the role of ORF3c as an immune evasion factor of SARS-CoV-2, inhibiting innate sensing in infected cells.
Mueller, Martin, et al. "ORF3c is expressed in SARS-CoV-2 infected cells and suppresses immune activation by inhibiting innate sensing." bioRxiv (2023): 2023-02.
Pubmed:
37870297
DOI:
10.15252/embr.202357137
Lamoot, Alexander. et al. "Lipid Nanoparticle Encapsulation Empowers Poly(I:C) to Activate Cytoplasmic RLRs and Thereby Increases Its Adjuvanticity." Small (Weinheim an der Bergstrasse, Germany), 2023.
Poly(I:C), a synthetic analogue of dsRNA, has been recognized as a potent activator of TLR3 and RLRs, including MDA-5 and RIG-I, as pathogen recognition receptors. However, its therapeutic use as a vaccine adjuvant is limited due to susceptibility to nucleases and low uptake by immune cells. To address these issues, the researchers encapsulated poly(I:C) into lipid nanoparticles (LNPs) containing an ionizable cationic lipid, allowing for electrostatic interactions with poly(I:C). LNP-formulated poly(I:C) was found to trigger both lysosomal TLR3 and cytoplasmic RLRs, and demonstrated superior innate immune activation, compared to unformulated poly(I:C). In addition, use of LNP-formulated poly(I:C) as an adjuvant for a recombinant full-length SARS-CoV-2 spike protein resulted in potent antibody production and complete protection against viral challenge in mouse models.
Lamoot, Alexander. et al. "Lipid Nanoparticle Encapsulation Empowers Poly(I:C) to Activate Cytoplasmic RLRs and Thereby Increases Its Adjuvanticity." Small (Weinheim an der Bergstrasse, Germany), 2023.
Pubmed:
37867244
DOI:
10.1002/smll.202306892