The ARHGEF28 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ARHGEF28 gene in the Jurkat T lymphocyte line. This product provides a heterogeneous mixture of cells with targeted gene disruptions, avoiding clonal selection biases and enabling robust population-level analysis. It serves as a loss-of-function model for investigating ARHGEF28 functions in T cell biology and leukemia. The polyclonal format ensures experimental reproducibility and is suitable for a wide range of functional assays.
The parental Jurkat cell line is an immortalized human T lymphocyte line derived from the peripheral blood of a 14-year-old boy with acute T cell leukemia. These cells are widely used to study T cell receptor (TCR) signaling, cytokine production, and apoptosis. Jurkat cells grow in suspension, retain key signaling pathways, and provide a tractable model for dissecting T cell-specific functions and leukemogenesis.
ARHGEF28 encodes a Rho guanine nucleotide exchange factor (GEF) that specifically activates RhoA by catalyzing GDP-to-GTP exchange. Upstream inputs include LPAR, thrombin receptors, integrin receptors, GPCRs, S1P receptors, and the TCR complex. Activated RhoA-GTP subsequently stimulates ROCK1/2 and LIMK, leading to phosphorylation of cofilin and regulation of actin polymerization, myosin light chain (MLC) activity, and F-actin stress fiber formation. ARHGEF28 also interacts with FAK, p120 catenin, and PDZ-domain proteins such as PICK1, providing mechanical coupling to adhesion sites.
In Jurkat T cells, ARHGEF28-mediated RhoA activation regulates cytoskeletal rearrangements downstream of TCR and LPA receptor signaling. Disruption of ARHGEF28 enables direct investigation of its role in F-actin dynamics, cell adhesion, and migration. Because RhoA pathway dysregulation is implicated in T cell leukemia progression and immune dysregulation, this model allows dissection of ARHGEF28-dependent leukemic cell phenotypes. The polyclonal knockout format avoids clonal selection artifacts and better represents population-level heterogeneity.
These knockout cells are suitable for diverse assays including Western blotting for active RhoA-GTP, immunofluorescence for F-actin structures, transwell migration assays, and cell adhesion assays. Flow cytometry can assess TCR activation markers, while co-immunoprecipitation and RNA-seq enable interaction mapping and transcriptomic profiling. Drug sensitivity testing with ROCK inhibitors (e.g., Y-27632) is feasible in high-throughput formats. For ordering, technical support, or custom requests, please contact Ascent Research.
