BICD2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte line, engineered to disrupt the BICD2 gene and generate a loss-of-function model. This polyclonal population consists of a pool of edited cells, providing a heterogeneous system to study BICD2-dependent intracellular transport processes in a human T cell context.
The Jurkat cell line, established from an acute T cell leukemia, is an immortalized human T lymphocyte model that recapitulates key aspects of T cell receptor (TCR) signaling, activation, and cytokine production. Widely employed in immunology and cancer biology, Jurkat cells offer a robust, genetically tractable system for investigating T cell biology and signal transduction.
BICD2 encodes a dynein cargo adaptor that mediates minus-end-directed transport along microtubules, linking diverse cargoes??including vesicles, mRNAs, and organelles??to the dynein motor complex. It directly interacts with the dynein heavy chain DYNC1H1 and the dynactin subunit p150Glued, while its recruitment to cargo is regulated by the GTPases RAB6A and RAB11A, as well as by GSK3-mediated phosphorylation. Downstream, BICD2 facilitates the trafficking of RAB6A-positive Golgi-derived vesicles, Staufen1-containing messenger ribonucleoproteins (mRNPs), and lipid droplets, thereby controlling organelle positioning, mRNA localization, and Golgi organization. Additionally, BICD2 forms complexes with SUN1 and SYNE/Nesprin proteins at the nuclear envelope, linking nuclear positioning to the cytoskeleton.
In Jurkat T cells, BICD2 knockout disrupts dynein-mediated transport pathways critical for immune function. Efficient TCR recycling, polarized secretion of cytokines at the immune synapse, and maintenance of surface receptor levels all depend on intact microtubule minus-end-directed trafficking. Loss of BICD2 therefore perturbs these processes, leading to altered T cell activation dynamics. This knockout model provides a valuable tool for dissecting the cytoskeletal and trafficking requirements of T cell responses, and the polyclonal nature of the population allows for the evaluation of functional heterogeneity arising from diverse editing events.
Researchers can use this product to investigate dynein-mediated transport in T lymphocytes, including the roles of BICD2 in TCR recycling and immune synapse organization. It is suitable for examining mRNA localization mechanisms via RNA-FISH, analyzing Golgi morphology through immunofluorescence, and studying disease mechanisms relevant to SMALED2 and hereditary spastic paraplegia. The model is also amenable to high-throughput screening for modulators of dynein-based transport. Typical assays include Western blotting for BICD2 and dynein components, co-immunoprecipitation with DYNC1H1 or dynactin, flow cytometry for surface receptor expression, and live-cell imaging of lysosomal trafficking. For further information or ordering, contact Ascent Research.
