In Stock Cell Lines
Mus musculus (Mouse)
Ascites
Adherent
The Sh2d3c Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout model in murine macrophages, enabling loss-of-function studies of the adaptor protein NSP3/Chat. This cell line targets Sh2d3c, a scaffold that bridges integrin and TCR signaling to the actin cytoskeleton by interacting with p130Cas and Crk following phosphorylation by Src family kinases. In the RAW 264.7 macrophage host, Sh2d3c regulates adhesion, migration, and phagocytosis. Knockout of Sh2d3c facilitates investigation of integrin-dependent macrophage functions relevant to inflammation, autoimmune disorders, and cancer metastasis, using assays such as Transwell migration, adhesion, and phagocytosis assays.
TSC22D3 Knockout Jurkat E6.1 Cell Line
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HECA Knockout Hela Polyclonal Cells
Cat. No. ARG25544
CD58 Knockout 22RV-1 Polyclonal Cells
Cat. No. ARG43657
LIMCH1 Knockout 786-O Polyclonal Cells
Cat. No. ARG5704
LRRFIP2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4389
The Sh2d3c Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line that provides a targeted disruption of the Sh2d3c gene in a murine macrophage background. This model serves as a loss-of-function system for dissecting the roles of Sh2d3c in integrin-mediated adhesion, migration, and cytoskeletal reorganization. The knockout cell line is derived from the well-characterized RAW 264.7 macrophage line, enabling researchers to examine Sh2d3c-dependent signaling in an innate immune context.
RAW 264.7 is a murine macrophage cell line originally derived from BALB/c mice, widely adopted for studies of macrophage biology due to its functional responsiveness to lipopolysaccharide (LPS) and its capacity for phagocytosis, antigen presentation, and production of inflammatory cytokines such as TNF-?? and IL-6. These features make it a relevant model for investigating innate immune mechanisms, host-pathogen interactions, and inflammatory responses.
Sh2d3c encodes the adaptor protein NSP3/Chat, which serves as a molecular scaffold linking integrin and T cell receptor (TCR) signaling to the actin cytoskeleton. Following integrin ligation or TCR engagement, Src family kinases such as Lck and Fyn phosphorylate Sh2d3c, facilitating its interaction with p130Cas (BCAR1) and Crk. This assembly promotes the activation of Rac1, leading to actin polymerization, focal adhesion turnover, and enhanced cell migration. By coordinating these events, Sh2d3c operates downstream of integrin receptors, chemokine receptors, and FAK to regulate adhesion and motility.
In macrophages, Sh2d3c-mediated signaling is implicated in the regulation of integrin-dependent adhesion, migration, and phagocytosis??processes essential for tissue surveillance, wound healing, and immune effector functions. Disruption of Sh2d3c in the RAW 264.7 background allows for the direct assessment of its contribution to macrophage motility, phagocytic uptake, and integrin signaling dynamics. This knockout model is therefore valuable for studying inflammatory disorders, autoimmune diseases, and tumor-associated macrophage behavior relevant to cancer metastasis.
This cell line supports a range of functional assays to interrogate Sh2d3c biology, including Transwell migration assays, adhesion assays on extracellular matrix substrates, and phagocytosis assays using fluorescent particles or bacteria. Downstream signaling can be examined by western blotting for phosphorylated FAK and p130Cas, while immunofluorescence microscopy reveals actin cytoskeletal organization. Flow cytometry enables quantification of integrin surface expression, and co-immunoprecipitation can confirm disrupted Sh2d3c-p130Cas complexes. The Sh2d3c Knockout RAW 264.7 Cell Line thus provides a robust platform for dissecting macrophage integrin signaling pathways with potential translational implications in immune dysfunction and cancer. For further information, please contact Ascent Research.
