The ANK3 Knockout Jurkat Polyclonal Cells product comprises a polyclonal population of Jurkat T-lymphoblastoid cells engineered via CRISPR/Cas9-mediated gene disruption to generate a loss-of-function model for the ANK3 gene. This polyclonal knockout format provides a heterogeneous pool of edited cells, reflecting a range of genetic modifications at the target locus, and is suitable for functional studies without clonal selection. The product enables investigation of ankyrin-G-dependent processes in a T-cell context, offering a versatile tool for studying membrane-cytoskeletal interactions and adhesion signaling.
The host cell line, Jurkat, is an immortalized human T lymphoblastoid line originally derived from an acute T cell leukemia patient. Jurkat cells are widely employed as a model system for T cell receptor (TCR) signaling, leukemia biology, and immunological synapse formation. Their robust growth characteristics and well-characterized signaling pathways make them an ideal host for knockout studies. In this polyclonal ANK3 knockout background, Jurkat cells retain their lymphoblastoid morphology and key TCR-responsive elements, enabling direct assessment of ankyrin-G function in lymphocyte physiology.
ANK3 encodes ankyrin-G, a large scaffold protein that tethers integral membrane proteins to the underlying spectrin-actin cytoskeleton. Mechanistically, ankyrin-G interacts directly with ??-spectrin and F-actin to organize cortical membrane domains, while binding cell adhesion molecules such as CD44, neurofascin, and L1CAM, as well as voltage-gated sodium channels (e.g., Nav1.6) and KV7.2/7.3 potassium channels. In T cells, ANK3 expression is upregulated by TCR activation and downstream calcium/calcineurin/NFAT signaling, and is also influenced by Wnt/??-catenin pathways. Ankyrin-G thereby coordinates the localization of adhesion receptors and ion channels at the plasma membrane, facilitating immunological synapse assembly, cell polarization, and migration.
In the Jurkat T-cell context, disruption of ANK3 perturbs the linkage between CD44 and the cortical actin network, potentially impairing T-cell adhesion, spreading, and synapse formation. This knockout model is thus valuable for dissecting the cytoskeletal basis of T-cell activation and motility. Moreover, given the strong genetic association of ANK3 variants with bipolar disorder, schizophrenia, and autism spectrum disorders, the Jurkat ANK3 knockout cells can serve as a peripheral cellular model to explore shared neuropsychiatric disease mechanisms involving ankyrin-G dysfunction, including altered protein localization and signaling.
Researchers can apply this polyclonal knockout population to a broad range of experimental workflows. Typical applications include adhesion and migration assays to examine CD44-dependent lymphocyte trafficking, immunofluorescence and live-cell imaging to assess cytoskeletal organization and receptor clustering, and co-immunoprecipitation or Western blotting to map ankyrin-G interaction networks. The cells are also suitable for drug screening targeting ankyrin-G-related pathways in neuropsychiatric conditions, and for electrophysiological recordings to study ion channel surface expression. For technical inquiries, please contact Ascent Research.
