In Stock Cell Lines
Mus musculus (Mouse)
Ascites
Adherent
The S100a4 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited macrophage knockout model for studying the calcium-binding protein S100a4. S100a4 interacts with non-muscle myosin IIA and actin to regulate cell migration, invasion, and epithelial-mesenchymal transition, and it is transcriptionally induced by TGF-??, TNF-??, and Wnt signaling. This model enables investigation of macrophage-driven metastasis, fibrosis, and inflammation. In the RAW 264.7 murine macrophage background, S100a4 knockout allows dissection of its roles in cytokine production, phagocytosis, and tumor microenvironment modulation. Applications include Transwell migration and invasion assays, NF-??B reporter assays, and drug screening for anti-metastatic and anti-fibrotic therapies.
PARD6B Knockout HT29 Polyclonal Cells
Cat. No. ARG14603
PARVB Knockout HT29 Polyclonal Cells
Cat. No. ARG13925
ANAPC7 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30321
HSD17B12 Knockout HT29 Polyclonal Cells
Cat. No. ARG33384
FOXJ2 Knockout Raji Polyclonal Cells
Cat. No. ARG1986
Mouse Corneal Endothelial Cells
Cat. No. ARP0643
The S100a4 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse macrophage-like RAW 264.7 line. This product provides a loss-of-function model for S100a4, achieved through CRISPR/Cas9-mediated gene disruption. S100a4 encodes a calcium-binding protein that modulates migration, invasion, and cytoskeletal remodeling. The knockout cell line enables precise investigation of S100a4 function in macrophage biology without ectopic sequences. It is supplied as a ready-to-culture cell line for a broad range of assays.
The parental RAW 264.7 cell line is an Abelson murine leukemia virus-transformed macrophage line from BALB/c mice. These cells exhibit characteristic macrophage functions such as phagocytosis, cytokine production, and responsiveness to inflammatory stimuli. As an established model of immune effector cells, RAW 264.7 is widely used to study innate immunity, host-pathogen interactions, and macrophage roles in tissue remodeling and disease. The S100a4 knockout in this background allows dissection of the gene??s contributions to macrophage-mediated processes.
S100a4 functions as a calcium-dependent regulator of cytoskeletal dynamics by interacting with non-muscle myosin IIA, tropomyosin, and actin. It is transcriptionally upregulated by TGF-??, EGF, TNF-??, IL-6, and Wnt pathway activation, with NF-??B and AP-1 mediating its expression. Downstream, S100a4 promotes invasive and metastatic phenotypes through activation of MMP9, MMP2, VEGF, and suppression of p53. Its signaling involves Src, FAK, RhoA, ERK1/2, Snail, and Twist, which collectively drive EMT and cell motility. S100a4 also interacts with RAGE and Annexin II. Disruption of S100a4 in RAW 264.7 cells impairs these networks, affecting macrophage migration and cytokine output.
In macrophages, S100a4 tunes the tumor microenvironment, fibrotic responses, and chronic inflammation. RAW 264.7 cells expressing S100a4 contribute to matrix remodeling and immune cell recruitment; its knockout attenuates these effector functions. This model is critical for understanding how macrophage-derived S100a4 influences cancer metastasis, pulmonary and renal fibrosis, and inflammatory diseases such as rheumatoid arthritis. Eliminating S100a4 allows direct testing of macrophage-specific loss in disease progression.
The S100a4 Knockout RAW 264.7 Cell Line is ideal for studying macrophage roles in tumor cell invasion, screening for compounds that block S100a4-dependent metastasis, and investigating fibrosis mechanisms. Assays include Western blotting, RT-qPCR, Transwell migration/invasion, immunofluorescence for cytoskeletal organization, ELISA for cytokine secretion, flow cytometry, co-immunoprecipitation, and NF-??B reporter assays. This knockout model accelerates mechanistic studies and drug discovery targeting S100a4 in macrophage-driven pathologies. For further information, please contact Ascent Research.
