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.
PEX5 Knockout K562 Polyclonal Cells
Cat. No. ARG19380
MTX3 Knockout jurkat Polyclonal Cells
Cat. No. ARG12935
FZD2 Knockout jurkat Polyclonal Cells
Cat. No. ARG12915
PAK1 Knockout CAL27 Polyclonal Cells
Cat. No. ARG11544
JAG2 Knockout K562 Polyclonal Cells
Cat. No. ARG20726
IRF2 Knockout AGS Polyclonal Cells
Cat. No. ARG27053
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.
