ARHGEF12 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T lymphocyte cell line. This product provides a heterogeneous pool of cells with disrupted ARHGEF12 gene function, enabling population-level assessment of gene perturbation effects without clonal selection bias. Compared to clonal lines, the polyclonal format better reflects the diversity of editing outcomes, making it a versatile tool for functional genomics and phenotypic screens.
The Jurkat cell line is a widely used human T lymphocyte model derived from the peripheral blood of a 14-year-old boy with acute T cell leukemia. Immortalized and adapted to suspension culture, Jurkat cells retain key features of activated T cells, including robust T cell receptor (TCR) signaling, cytokine production, and antigen-induced apoptosis. They are extensively employed in immunological research to study T cell activation, differentiation, and leukemogenesis. Their genetic tractability makes them an ideal host for CRISPR/Cas9-mediated gene editing, enabling targeted disruption of genes like ARHGEF12 to dissect T cell biology and cancer mechanisms.
ARHGEF12 encodes a Rho guanine nucleotide exchange factor (GEF) that activates the small GTPase RhoA by catalyzing GDP/GTP exchange. Active RhoA-GTP engages downstream effectors ROCK1/2, which phosphorylate MYL2 to drive actomyosin contractility and formation of actin stress fibers and focal adhesions. Upstream, ARHGEF12 is regulated by G12/13-coupled GPCRs, integrin adhesion, TGF-??, and mechanical force, integrating diverse signals to reorganize the cytoskeleton. The protein also interacts with CTNNB1, PDLIM5, and SLC9A3R1, linking RhoA signaling to other cellular processes.
In Jurkat T cells, ARHGEF12-dependent RhoA activation is critical for processes requiring actin remodeling, such as immunological synapse formation, migration, and integrin-mediated adhesion. Disruption of ARHGEF12 is anticipated to impair RhoA-driven actin polymerization, potentially affecting T cell activation, motility, and adhesion. Given the leukemic origin of Jurkat cells, this knockout model facilitates investigation of ARHGEF12 in leukemic cell dissemination and survival. The polyclonal population offers a physiologically relevant platform to study the role of this GEF in both normal T cell biology and hematological malignancy.
This ARHGEF12 knockout pool supports a wide array of functional studies, including RhoA GTPase activation assays (G-LISA or pull-down), phalloidin staining for F-actin, Transwell migration and invasion assays, and flow cytometry for adhesion markers or activation status. Adhesion assays can probe integrin-mediated attachment, while phospho-specific antibodies against ROCK1 and MYL2 enable signaling pathway analysis. The model is also suitable for drug screening targeting the RhoA-ROCK axis. For additional technical information or custom orders, please contact Ascent Research.
