The Mapk7 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered for targeted disruption of the Mapk7 gene in a murine macrophage background. This product provides a stable loss-of-function model for investigating ERK5 (MAPK7) signaling without relying on transient or pharmacological approaches. The cell line is supplied as an adherent culture, ready for expansion and downstream experimental manipulation. By eliminating endogenous Mapk7 expression, researchers can directly assess the kinase’s contributions to macrophage biology, signal transduction, and disease-relevant processes.
The host cell line, RAW 264.7, is a well-established, macrophage-like line derived from ascites of a BALB/c mouse following Abelson leukemia virus infection. These cells function as professional phagocytes and are widely utilized to study innate immune responses, antigen presentation, and inflammatory mediator production. Their adherent growth, rapid doubling time, and responsiveness to TLR ligands, cytokines, and stress stimuli make RAW 264.7 cells a versatile platform for mechanistic studies in immunology and cell biology. The Mapk7 knockout in this context enables dissection of ERK5-specific roles in macrophage activation, survival, and effector functions.
MAPK7 (ERK5) is a mitogen-activated protein kinase that mediates cellular responses to growth factors, cytokines, and environmental stress. It is activated through dual phosphorylation on its TEY motif by the upstream kinase MAP2K5 (MEK5), which itself receives signals from MEKK2 or MEKK3 in response to EGF, VEGF, oxidative stress, or hyperosmolarity. Upon activation, ERK5 translocates to the nucleus where it phosphorylates and activates transcription factors such as MEF2C, MEF2D, and Sap1a, thereby driving expression of target genes including c-Fos, c-Myc, Egr-1, and cyclin D1. ERK5 also interacts with actin cytoskeleton components and heat shock protein 27, linking kinase signaling to cytoskeletal dynamics. This positions MAPK7 at the intersection of the MAPK, PI3K-Akt, Ras, VEGF, NF-kappa B, and p53 pathways, integrating diverse inputs to control proliferation, differentiation, and stress adaptation.
In the RAW 264.7 macrophage model, ERK5 signaling is critical for modulating inflammatory responses and maintaining cell survival under stress. The Mapk7 Knockout RAW 264.7 Cell Line enables precise investigation of how ERK5 controls cytokine secretion, phagocytic activity, and surface marker expression in innate immune cells. It also facilitates studies on the kinase’s role in macrophage polarization, LPS signaling, and apoptosis regulation. By comparing knockout and wild-type responses, researchers can identify ERK5-dependent transcriptional programs and signaling nodes that are essential for macrophage function in health and disease.
This knockout cell line is suited for a broad range of experimental applications, including cancer research, cardiovascular disease modeling, inflammation studies, and metabolic disorder investigations. Representative assays include western blotting to assess phospho-ERK5 and downstream targets like MEF2C, RT-qPCR for transcriptional readouts, flow cytometry for surface activation markers and Annexin V staining, ELISA for cytokine quantification, and functional phagocytosis or cell proliferation assays. The model also supports phospho-signaling pathway analysis and RNA-seq-based transcriptomic profiling. For further inquiries or technical support, please contact Ascent Research.
