The ADD3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human ADD3 gene in Jurkat T lymphocytes. This product provides a heterogeneous loss-of-function model generated by CRISPR-mediated disruption of ADD3, enabling researchers to study gamma-adducin function in a T cell context without clonal isolation. The polyclonal format captures a range of knockout efficiencies and allows population-level functional assays, making it suitable for exploring actin cytoskeleton dynamics and cell adhesion mechanisms.
The Jurkat E6-1 host cell line is an immortalized human T lymphocyte model derived from the peripheral blood of a 14-year-old male with acute T cell leukemia. Jurkat cells are widely employed in research on T cell receptor signaling, HIV infection, and apoptosis. Their robust and well-characterized signaling networks, including those governing actin remodeling, provide a relevant background for investigating the cytoskeletal roles of gamma-adducin in immune cell function and malignant transformation.
ADD3 encodes gamma-adducin, an actin-spectrin cytoskeletal linker that caps and stabilizes actin filaments by recruiting spectrin (SPTBN1), thereby organizing the membrane-associated cytoskeleton. Gamma-adducin is modulated by upstream regulators including PKA, PKC, RhoA/ROCK, and calcium/calmodulin. It interacts with actin, spectrin, ADD1, ADD2, calmodulin, and PKC, and participates in focal adhesion, tight junction, and Rho GTPase signaling. Through these interactions, ADD3 governs cell adhesion, migration, and membrane stability.
In Jurkat T cells, disruption of ADD3 perturbs the actin-spectrin network, leading to impaired cell adhesion and migration. This knockout model may also affect immunological synapse formation, a process critical for T cell activation. By eliminating gamma-adducin, researchers can dissect how the membrane-associated cytoskeleton influences T lymphocyte signaling, polarization, and motility, while also modeling aspects of neurodevelopmental disorders and cancer biology where adducin dysfunction is implicated.
This polyclonal knockout cell population is well-suited for T cell activation studies, cytoskeletal dynamics in lymphocytes, leukemia cell migration and invasion assays, and drug screening targeting cytoskeletal pathways. Representative experimental techniques include Western blotting, immunofluorescence, flow cytometry, Transwell migration assays, adhesion assays, phalloidin staining, phospho-kinase profiling, and RNA-seq. For additional information, please contact Ascent Research.
