Genome-edited Cells
Ascites
The Il1rap Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse RAW 264.7 macrophage line, in which the Il1rap gene has been disrupted. IL1RAP is an essential co-receptor for IL-1R1 and ST2, mediating pro-inflammatory signaling through MYD88, IRAK kinases, and downstream NF-??B and MAPK pathways. This knockout model is ideal for dissecting IL-1 and IL-33 signaling in macrophages, studying inflammatory cytokine regulation, and screening for pathway antagonists. Key applications include western blotting for phosphorylated signaling intermediates, RT-qPCR, ELISA, and functional innate immune assays, making it a valuable tool for autoimmune and inflammatory disease research.
LRP1 Knockout Lovo Polyclonal Cells
Cat. No. ARG11730
ADA Knockout huh-7 Polyclonal Cells
Cat. No. ARG27802
ADD3 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30239
CRBN Knockout MES-OV Polyclonal Cells
Cat. No. ARG6552
NBN Knockout 786-O Polyclonal Cells
Cat. No. ARG5519
LRP6 Knockout AGS Polyclonal Cells
Cat. No. ARG3158
The Il1rap Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse RAW 264.7 macrophage line, in which the Il1rap gene has been disrupted to create a stable loss-of-function model. This genetic modification eliminates expression of the essential co-receptor required for IL-1 receptor 1 (IL-1R1) and ST2 signaling, enabling precise interrogation of IL-1??, IL-1??, and IL-33 pathways in innate immunity.
The parental RAW 264.7 line, originally established from an Abelson leukemia virus-induced tumor in a BALB/c mouse, is a widely used macrophage model characterized by phagocytic activity, robust production of inflammatory cytokines such as TNF-?? and IL-6, and antigen presentation capabilities. These cells are highly responsive to toll-like receptor ligands and serve as a well-established system for studying macrophage biology and inflammatory signaling.
IL1RAP functions as an obligate co-receptor that forms heterodimers with IL-1R1 to mediate responses to IL-1?? and IL-1??, and with ST2 for IL-33 signaling. Upon ligand engagement, IL1RAP facilitates the recruitment of the adaptor MYD88 and the kinases IRAK1 and IRAK4, which in turn activate TRAF6. This triggers downstream IKK complex-mediated NF-??B activation and MAPK cascades involving p38, JNK, and ERK, leading to transcription of pro-inflammatory genes including Il6, Tnf, and Il1b. Regulatory proteins such as Tollip and SIGIRR interact with the receptor complex to fine-tune signaling output.
In the RAW 264.7 background, Il1rap knockout enables researchers to distinguish between IL-1/IL-33-dependent and -independent pathways in macrophage responses. This model is especially relevant for dissecting the molecular mechanisms of inflammatory diseases, including rheumatoid arthritis, psoriasis, and inflammatory bowel disease, where dysregulated IL-1 or IL-33 signaling contributes to pathogenesis.
This knockout cell line supports a range of assays: western blotting for phosphorylated NF-??B p65, p38, JNK, and ERK; RT-qPCR for Il6, Tnf, and Il1b transcripts; ELISA for secreted TNF-?? and IL-6; NF-??B luciferase reporter assays; flow cytometry for intracellular cytokines; and macrophage phagocytosis assays. It is also suited for small-molecule inhibitor screens targeting IL-1 pathway components and for evaluating therapeutic candidates in autoinflammatory disease models. For additional information, please contact Ascent Research.
