RAW-Lucia™ ISG-KO-IRF5 Cells
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Cat.code:
rawl-koirf5
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ABOUT
IRF5 knockout reporter macrophages
RAW-Lucia™ ISG-KO-IRF5 cells were generated from the RAW-Lucia™ ISG cell line through the stable knockout of the IRF5 gene.
Interferon regulatory receptor 5 (IRF5) is a transcription factor involved in the induction of type I interferon (IFN) downstream of pattern recognition receptors (PRRs), including the cytosolic nucleic acid sensors [1, 2]. There is increasing evidence that IRF5 plays a key role in numerous inflammatory and autoimmune diseases, including rheumatoid arthritis (RA) and inflammatory bowel disease [1, 3]. Importantly, because IRF5 acts in a cell-type and activity-specific manner, it is an attractive therapeutic target [1].
RAW-Lucia™ ISG-KO-IRF5 cells feature a Lucia luciferase reporter gene under the control of an ISG54 promoter enhanced by multimeric ISREs. Activation of the IRF pathway can be readily assessed by monitoring the activity of the secreted Lucia luciferase in the supernatant using the QUANTI-Luc™ 4 Lucia/Gaussia detection reagent. A differential response between RAW-Lucia™ ISG-KO-IRF5 cells and their parental cells is observed when using DNA- or RNA-based agonists with distinct transfection reagents (see Figures). RAW-Lucia™ ISG-KO-IRF5 cells retain the full ability to respond to type I interferons (IFN-α and IFN-β) and lipopolysaccharide (a TLR4 agonist) (see Figures).
Features:
- Verified knockout of the IRF5 gene (PCR, DNA sequencing, and Western blot)
- Functionally validated with a selection of PRR ligands and cytokines
- Readily assessable Lucia luciferase activity
Applications:
- Defining the role of IRF5 in PRR-induced signaling
- Highlighting possible overlapping PRR activation, or regulatory mechanisms
References:
1. Almuttaqi, H. & Udalova, I.A. 2019. Advances and challenges in targeting IRF5, a key regulator of inflammation. FEBS J 286, 1624-1637.
2. Zhao G-N. et al., 2015. Interferon regulatory factors: at the crossroads of immunity, metabolism, and disease. Biochim Biophys Acta. 2015 Feb;1852(2):365-78.
3. Kaur, A. et al. 2018. IRF5-mediated immune responses and its implications in immunological disorders. Int Rev Immunol 37, 229-248.
Disclaimer: These cells are for internal research use only and are covered by a Limited Use License (See Terms and Conditions). Additional rights may be available.
SPECIFICATIONS
Specifications
Defining the role of IRF5 in PRR-induced signaling, Highlighting possible overlapping PRR activation, or regulatory mechanisms
Complete DMEM (see TDS)
Verified using PlasmotestTM
Each lot is functionally tested and validated.
CONTENTS
Contents
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Product:RAW-Lucia™ ISG-KO-IRF5 Cells
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Cat code:rawl-koirf5
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Quantity:3-7 x 10^6 cells
- 1 ml of Normocin™ (50 mg/ml)
- 1 ml of Zeocin® (100 mg/ml)
- 1 tube of QUANTI-Luc™ 4 Reagent (sufficient to prepare 25 ml)
Shipping & Storage
- Shipping method: Dry ice
- Liquid nitrogen vapor
- Upon receipt, store immediately in liquid nitrogen vapor. Do not store cell vials at -80°C.
Storage:
Caution:
Details
IRF5 background
Interferon regulatory factor 5 (IRF5) is a transcription factor that plays a central role in inflammation. It mediates the induction of type I interferons (IFNs) and proinflammatory cytokines through binding to ISRE and NF-κB motifs, respectively [1]. IRF5 has been implicated downstream of pattern recognition receptors (PRRs), including the cytosolic DNA/cyclic dinucleotide sensors cGAS/STING, the cytoplasmic RNA sensors, RIG-I and MDA5, Toll-like receptors (TLRs), the NOD-like receptor NOD2, and C-type lectin receptors such as Dectin 1 and Dectin 2 [1, 2]. Depending on the PRR that is triggered, IRF5 is activated through distinct mechanisms. TLR stimulation elicits IRF5 activation downstream of the MyD88 or the TRIF adaptors. Nucleic acid sensing by RIG-I, MDA5, cGAS or STING, elicits IRF5 activation through TBK1 (TANK-binding kinase 1). IRF5 can also be activated by the IKKβ kinase downstream of the MAVS adaptor associated with RIG-I or MDA5 [2]. IRF5 plays a key role in numerous inflammatory and autoimmune diseases including rheumatoid arthritis (RA) and inflammatory bowel disease [1, 3]. Importantly, because IRF5 acts in a cell-type and activity-specific manner, it is an attractive therapeutic target [1].
1. Almuttaqi, H. & Udalova, I.A. 2019. Advances and challenges in targeting IRF5, a key regulator of inflammation. FEBS J 286, 1624-1637.
2. Zhao, G.N. et al. 2015. Interferon regulatory factors: at the crossroads of immunity, metabolism, and disease. Biochim Biophys Acta. 2015 Feb;1852(2):365-78.
3. Kaur, A. et al. 2018. IRF5-mediated immune responses and its implications in immunological disorders. Int Rev Immunol 37, 229-248.
DOCUMENTS
Documents
Technical Data Sheet
Validation Data Sheet
Safety Data Sheet
Certificate of analysis
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