RLR Reporter Cells
InvivoGen offers various human and mouse cell lines to study RLR signaling pathways.
Example of RLR-reporter cell line
(click to enlarge)
RLRs (RIG-I-like receptors) are a family of three cytoplasmic RNA helicases that are critical for the effective immune response against viruses through the sensing of cytoplasmic RNA.
RIG-I (retinoic-acid-inducible protein 1) and MDA5 (melanoma-differentiation-associated gene 5) sense double-stranded RNA (dsRNA), a replication intermediate for RNA viruses. LGP2 (aka DHX58) contains an RNA binding domain but acts as a negative feedback regulator of RIG-I and MDA5. Typically, activated RIG-I or MDA5 are recruited by the adaptor protein MAVS (mitochondrial antiviral signaling protein, aka IPS1 or VISA), leading to IFN regulatory factor (IRF3 and IRF7)-dependent type I IFN production and NF-κB-dependent inflammatory cytokine production.
To facilitate the monitoring of RLR-mediated responses, InvivoGen has developed:
– IRF-reporter cell lines
– NF-κB and IRF-reporter cell lines
These cell lines are extensively tested for viability, stability, biological activity, and absence of mycoplasma to ensure strong and reproducible results. Moreover, we provide detailed handling and experimental procedures for all cell lines, to minimize the need for optimization or troubleshooting by the end-user.
Depending on your research needs, you may choose from:
- Human or mouse cell lines
- SEAP (secreted embryonic alkaline phosphatase) and/or Lucia luciferase reporters
- Cell lines deficient for functional RIG-I, MDA5, or MAVS
- Cells lines overexpressing the human RIG-I
The activity of the reporter proteins, SEAP and Lucia luciferase, can be conveniently assayed in the cell supernatants using the SEAP detection reagents QUANTI-Blue™ Solution and the Lucia luciferase detection reagent, QUANTI-Luc™ 4 Lucia/Gaussia.
InvivoGen also offers a comprehensive collection of STING products, including RLR ligands, RLR pathway inhibitors, and cloned RLR and related genes into an expression plasmid.