The ARHGEF16 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the ARHGEF16 gene, which encodes a guanine nucleotide exchange factor for Rho family GTPases. This product provides a genetically modified T-lymphoblast model derived from the Jurkat cell line, specifically intended for functional investigation of ARHGEF16 in Homo sapiens. The polyclonal knockout format ensures a heterogeneous pool of edited cells, facilitating robust gene function analyses without artifacts associated with single-cell clonal selection.
Jurkat cells are an immortalized human T lymphocyte cell line originally isolated from a 14-year-old male with acute lymphoblastic leukemia. This well-characterized line is extensively utilized as a model for studying T-cell receptor (TCR) signaling, T-cell activation, and acute T-cell leukemia pathogenesis. Jurkat cells express essential TCR signaling components, including the CD3 complex and the CD28 co-stimulatory receptor, thereby providing a relevant context for examining early events in immune receptor transduction and leukemogenesis.
ARHGEF16 functions as a guanine nucleotide exchange factor (GEF) that activates Rho family GTPases, primarily RhoA and Rac1, through GDP/GTP exchange. Downstream effectors such as ROCK, LIMK, cofilin, and the ARP2/3 complex then regulate actin cytoskeleton organization, cell migration, and adhesion. Within Jurkat T cells, ARHGEF16 is stimulated by upstream signals from the TCR/CD3 complex, CD28 co-stimulation, and the proximal tyrosine kinases Lck and Vav1. Upon activation, ARHGEF16 interacts with GDP-bound RhoA and Rac1, promoting their transition to active GTP-bound states that drive actin polymerization and focal adhesion turnover. Consequently, ARHGEF16 critically links TCR-mediated signaling to dynamic cytoskeletal remodeling.
Disruption of ARHGEF16 in this polyclonal knockout model impairs Rho GTPase-driven cytoskeletal rearrangements essential for T-cell spreading, migration, and adhesion. Given the pivotal role of Rho GTPase signaling in TCR responses, this model is highly pertinent for dissecting molecular mechanisms governing immune cell activation and effector functions. Because Jurkat cells serve as a standard acute T-cell leukemia model, ARHGEF16 knockout cells also enable exploration of how Rho signaling contributes to leukemic cell proliferation, survival, and invasion. Additionally, this model offers insights into inflammatory and autoimmune diseases such as inflammatory bowel disease and multiple sclerosis, where aberrant T-cell migration and adhesion are involved.
ARHGEF16 Knockout Jurkat Polyclonal Cells are applicable to diverse research fields, including T-cell biology, cancer biology, immunology, cytoskeletal dynamics, and drug target discovery. Standard molecular assays like Western blotting, RT-qPCR, and immunofluorescence can confirm target gene disruption and downstream signaling changes. Functional analyses may employ cell migration assays, adhesion assays, Rho GTPase activation assays, and flow cytometry to evaluate cytoskeletal dynamics and integrin-mediated adhesion. Phospho-signaling analysis further reveals the impact of ARHGEF16 loss on TCR-proximal kinase activity. This product serves as an essential reagent for studies integrating immune receptor signaling with actin cytoskeleton regulation, especially in leukemia and inflammatory disease contexts. For additional technical information and assistance, please contact Ascent Research.
