In Stock Cell Lines
Mus musculus (Mouse)
Ascites
Adherent
The Maf Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse macrophage line RAW 264.7. It abolishes expression of c-Maf, a transcription factor that promotes M2 macrophage polarization via the IL-4/STAT6 signaling axis and regulates key target genes such as Il10, Arg1, and Cd206. This model enables functional studies of macrophage polarization, cytokine signaling, and transcriptional networks. It is suited for investigating anti-inflammatory pathways, tumor microenvironments, and drug screening for M2 polarization inhibitors using assays such as RT-qPCR, flow cytometry, and ELISA.
MMP13 Knockout A2780 Polyclonal Cells
Cat. No. ARG18590
Immortalized Mouse Intestinal Stromal Cell
Cat. No. ARI0261
IFI30 Knockout A2780 Polyclonal Cells
Cat. No. ARG29184
KIAA0586 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG30111
ARHGEF6 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG32254
LILRB4 Knockout 786O Polyclonal Cells
Cat. No. ARG4748
The Maf Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line that disrupts the Maf gene in the murine RAW 264.7 macrophage background, eliminating c-Maf transcription factor expression. This loss-of-function model enables targeted investigation of Maf-dependent gene regulation and its role in macrophage biology.
RAW 264.7 cells, derived from BALB/c mouse peritoneal macrophages transformed with Abelson murine leukemia virus, provide a well-established macrophage model exhibiting phagocytic activity, antigen presentation, and robust cytokine responses. Their genetic tractability makes them ideal for studying signaling pathways that control macrophage activation and functional polarization.
c-Maf is a basic leucine zipper transcription factor that acts downstream of interleukin-4 (IL-4) to drive anti-inflammatory macrophage polarization. Upon IL-4 binding to its receptor, JAK1 phosphorylates STAT6, which translocates to the nucleus and induces c-Maf expression along with co-regulators PPAR?? and KLF4. c-Maf then dimerizes with AP-1 components (Jun, Fos) and recruits coactivators such as CBP/p300 and NFATc1 to activate transcription of M2-associated genes, including Il10, Arg1, Cd206, and Il4, while also integrating upstream signals from NF-??B and ERK pathways.
In RAW 264.7 macrophages, c-Maf is critical for IL-4-mediated alternative activation and M2 polarization, marked by upregulated arginase activity and scavenger receptor expression. Maf knockout impairs this transcriptional program, disrupting the induction of M2 markers and potentially skewing responses toward classical activation. Thus, this knockout serves as a powerful tool to dissect the transcriptional control of macrophage plasticity in inflammation, tumor microenvironments, and autoimmune settings.
Researchers can employ this cell line for RT-qPCR quantification of M2 effectors (e.g., Il10, Arg1, Cd206), western blotting of c-Maf and phospho-STAT6, flow cytometry for CD206 and F4/80 surface staining, and ELISA-based measurement of IL-10 and IL-4. Luciferase reporter assays enable assessment of Maf transactivation, while co-immunoprecipitation probes interactions with Jun/Fos complexes. These applications facilitate drug screening for M2 polarization inhibitors, analysis of tumor-associated macrophage biology, and validation of upstream IL-4/JAK/STAT signaling components. For additional information, contact Ascent Research.
