The ABLIM2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the ABLIM2 gene has been disrupted in Jurkat human T lymphocytes. This polyclonal format provides a heterogeneous pool of edited cells, avoiding the limitations of clonal selection, and is suited for functional studies of ABLIM2’s role in T cell biology.
The Jurkat cell line is an immortalized human T lymphocyte line derived from a 14-year-old male with T cell acute lymphoblastic leukemia (T-ALL). Widely used to study T cell signaling, immune responses, and leukemia, Jurkat cells offer a well-characterized model for examining actin-dependent processes relevant to T cell function and malignancy.
ABLIM2 encodes an actin-binding protein with LIM domains that links the actin cytoskeleton to focal adhesion components, including F-actin, vinculin, paxillin, and alpha-actinin. It is activated by Rho family GTPases (RhoA, Rac1, Cdc42), integrin receptors, and TGF-beta, and regulates actin filament assembly, focal adhesion turnover, and cell migration. ABLIM2 operates downstream of the RhoA/ROCK/LIM kinase/cofilin signaling cascade. Disruption of ABLIM2 is predicted to impair cytoskeletal dynamics and adhesion strength.
In Jurkat cells, ABLIM2 knockout likely compromises T cell adhesion to extracellular matrix and antigen-presenting cells, attenuates chemotactic migration, and destabilizes immune synapse formation, potentially blunting T cell activation. Given the leukemic origin, this model is particularly relevant for probing ABLIM2’s role in T-ALL cell dissemination and metastasis, offering insights into how cytoskeletal perturbations impact leukemic progression.
Applications include transwell migration assays, F-actin immunofluorescence, flow cytometry-based activation markers, co-immunoprecipitation for protein interactions, and RNA-seq. These polyclonal knockout cells facilitate drug screening for inhibitors of T cell migration or leukemic invasion. For additional support, contact Ascent Research.
