The KIF21A Knockout Jurkat Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KIF21A gene in Homo sapiens. This polyclonal knockout model offers a heterogeneous pool of Jurkat T lymphocyte cells with targeted disruption of KIF21A, enabling loss-of-function studies without clonal isolation. The CRISPR/Cas9-mediated gene disruption generates a versatile cellular tool for investigating KIF21A-dependent processes in a human T cell context.
Jurkat cells are an immortalized T lymphocyte line derived from a patient with acute T cell leukemia. They serve as a widely used model system for T cell signaling, activation, and leukemogenesis. Their robust growth and well-characterized signaling pathways make them ideal for studying the functional consequences of gene knockouts on T cell biology, including receptor-mediated activation, cytokine production, and cytoskeletal dynamics.
KIF21A encodes a kinesin-family motor protein that powers microtubule-dependent transport of organelles and cargoes, notably mitochondria. KIF21A interacts with trafficking adaptors TRAK1 and TRAK2, as well as microtubule-associated proteins such as MAP1B, to coordinate intracellular motility. It functions in kinesin-mediated transport pathways that govern axonal guidance, cytoskeletal remodeling, and mitochondrial distribution. Disruption of KIF21A is predicted to impair the anterograde movement of mitochondria along microtubules, leading to altered subcellular localization and potential dysregulation of energy-dependent cellular processes.
In Jurkat T cells, KIF21A knockout is expected to disrupt kinesin-dependent intracellular transport, which may compromise mitochondrial trafficking and cytoskeletal reorganization essential for T cell function. Given that T cell activation, migration, and immune synapse formation rely on precise spatial distribution of organelles and dynamic cytoskeletal changes, this model allows researchers to dissect the role of KIF21A in these processes. The polyclonal population-based knockout approach permits assessment of overall gene function without clone-specific artifacts.
This knockout cell product is suited for investigating axonal transport, neurobiology, motor neuron diseases, and congenital fibrosis of the extraocular muscles type 1 (CFEOM). In T cell biology, it enables studies of signaling, activation, and migration. Verification can be performed via western blotting, RT-qPCR, and immunofluorescence for mitochondrial distribution. Functional assays include T cell activation, migration, and phospho-signaling analysis. For further details or custom models, contact Ascent Research.
