Genome-edited Cells
Ascites
The Clec7a Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited macrophage cell line with targeted disruption of the Clec7a gene, abrogating expression of the ??-glucan receptor Dectin-1. This knockout model enables investigation of innate immune signaling, fungal recognition, and inflammatory pathways in a RAW 264.7 background. Dectin-1 signals via Syk and the CARD9?CBCL10?CMALT1 complex to activate NF-??B and MAP kinases, driving cytokine production. Clec7a loss impairs ??-glucan responses, making the line ideal for antifungal studies, pathway analysis, and screening for Dectin-1 modulators in research on candidiasis, colitis, and autoimmune disorders.
PALM Knockout HT29 Polyclonal Cells
Cat. No. ARG14882
ARL6IP5 Knockout HGC-27 Polyclonal Cells
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IRGQ Knockout SK-HEP-1 Polyclonal Cells
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FHIT Knockout Hela Polyclonal Cells
Cat. No. ARG7613
Mouse Spinal Cord Microvascular Endothelial Cell Medium
Cat. No. ARM0602
SF188
Cat. No. ARC0809
The Clec7a Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the Clec7a gene in the murine RAW 264.7 macrophage background. This model eliminates Dectin-1 expression, the primary innate receptor for ??-glucan polysaccharides, enabling precise study of C-type lectin receptor signaling and ??-glucan?Cindependent macrophage responses.
RAW 264.7 is a BALB/c-derived Abelson virus-transformed macrophage line retaining phagocytic, antigen presentation, and cytokine production functions. Its responsiveness to diverse microbial ligands makes it a standard platform for innate immunity and inflammation research.
Clec7a encodes Dectin-1, which recognizes fungal ??-glucans and triggers Syk kinase activation through its ITAM motif. This initiates the CARD9?CBCL10?CMALT1 (CBM) complex, leading to NF-??B and MAPK (ERK, JNK, p38) activation and transcription of pro-inflammatory cytokines such as TNF, IL-6, IL-23, and IL-1??. Dectin-1 signals cooperatively with TLR2 and interacts with Vav1, PLC??2, and PKC??. Clec7a knockout thus disrupts the primary Syk-dependent pathway for ??-glucan?Cinduced innate immunity.
Loss of Dectin-1 in macrophages abolishes ??-glucan?Ctriggered phagocytosis, cytokine release, and inflammasome activation. This provides a clean background to probe Syk-independent signaling, TLR crosstalk, and macrophage contribution to inflammatory diseases including colitis and colitis-associated cancer, where ??-glucan sensing modifies disease outcomes.
Research applications encompass studying antifungal immunity against Candida and Aspergillus, dissecting Syk?CCARD9 signaling, and screening for pathway modulators. Common assays include ??-glucan?Cinduced cytokine ELISA, phagocytosis measurement, western blot for phospho-Syk, NF-??B and MAPK activation profiling, RT-qPCR for cytokine transcripts, and flow cytometry to confirm Dectin-1 ablation. For further details or custom services, please contact Ascent Research.
