In Stock Cell Lines
Mus musculus (Mouse)
Ascites
Adherent
The Ptpn6 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited murine macrophage line harboring a disruption in the Ptpn6 gene encoding SHP-1 phosphatase. SHP-1 dephosphorylates key signaling molecules such as Syk and JAK2, attenuating ITAM- and cytokine-driven pathways, and its loss leads to hyperinflammatory responses. This knockout model enables investigation of negative regulatory mechanisms in macrophages, with direct relevance to autoimmune disorders like lupus. Researchers can utilize the line for studies on inhibitory receptor signaling, anti-inflammatory drug screening, and tumor macrophage biology, using assays such as phospho-signaling analysis and cytokine profiling.
PHC2 Knockout jurkat Polyclonal Cells
Cat. No. ARG13336
AKR1B1 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG29478
KDM4B Knockout A2780 Polyclonal Cells
Cat. No. ARG29295
GSDMD Knockout TE1 Polyclonal Cells
Cat. No. ARG36852
GMPPA Knockout 786-O Polyclonal Cells
Cat. No. ARG5127
GMEB2 Knockout Raji Polyclonal Cells
Cat. No. ARG1844
The Ptpn6 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited murine macrophage cell line in which the Ptpn6 gene, encoding the Src homology 2 domain-containing protein tyrosine phosphatase SHP-1, has been disrupted. This loss-of-function model enables detailed investigation of SHP-1-mediated negative regulatory mechanisms in immune cell signaling. The cell line is derived from the widely utilized RAW 264.7 macrophage host, providing a consistent genetic background for comparative studies with wild-type controls.
The parental RAW 264.7 cell line originates from an Abelson murine leukemia virus-transformed mouse macrophage and is extensively employed as a model for macrophage biology, including phagocytosis, cytokine secretion, and inflammatory responses. These adherent cells retain key macrophage characteristics such as expression of F4/80 and Toll-like receptors, making them a robust platform for studying innate immune signaling cascades.
SHP-1 contains tandem N-terminal SH2 domains that recognize phosphorylated immunoreceptor tyrosine-based inhibitory motifs (ITIMs) on receptors like CD22 and PD-1, leading to phosphatase activation. Once recruited, SHP-1 dephosphorylates critical signaling intermediates including Syk, ZAP70, Vav1, and JAK2, thereby attenuating ITAM-mediated and cytokine receptor pathways. Consequently, SHP-1 negatively regulates JAK-STAT, NF-??B, and MAPK/ERK cascades downstream of receptors such as the T cell receptor, B cell receptor, and Fc??RI. Interacting partners such as Grb2, LAT, and SHIP1 further modulate signal termination. In macrophages, SHP-1 restrains pro-inflammatory transcriptional programs, limiting production of TNF-?? and IL-6.
In the context of RAW 264.7 macrophages, disruption of Ptpn6 mimics the hyperinflammatory state observed in motheaten mice, characterized by excessive myeloid activation and autoimmunity. This knockout model is therefore highly relevant for dissecting SHP-1??s role in controlling macrophage effector functions, including phagocytosis and cytokine output, and for exploring the molecular basis of autoimmune and inflammatory disorders such as systemic lupus erythematosus. It also provides a valuable tool for evaluating SHP-1-dependent inhibitory receptor pathways that are central to immune checkpoint regulation.
Researchers can employ this cell line in diverse experimental workflows, including western blotting for phospho-Syk and phospho-JAK2, NF-??B luciferase reporter assays, ELISA-based cytokine quantification, phagocytosis assays, and transcriptomic analysis via RNA-seq. Applications span investigation of inhibitory receptor signaling, anti-inflammatory drug target validation, tumor-associated macrophage reprogramming, and immune checkpoint therapy development. For further information and ordering, contact Ascent Research.
