The KIF13A Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T-lymphocyte line, in which the KIF13A gene encoding a plus-end-directed kinesin motor has been disrupted. This mixed population enables functional studies of KIF13A-dependent trafficking and cell division without clonal biases.
Jurkat cells are an immortalized human T lymphocyte line established from a patient with acute T-cell leukemia. These suspension cells are extensively used to model T-cell receptor signaling, cytokine production, and apoptosis. Their robust proliferation and well-defined signaling pathways render them a suitable host for investigating endosomal dynamics and lysosomal enzyme secretion in a malignant lymphoid context.
KIF13A transports mannose-6-phosphate receptor (M6PR)-containing vesicles from the trans-Golgi network to the plasma membrane via interaction with the AP-1 adaptor complex (??-adaptin subunit). This trafficking is regulated by Arf1 GTPase and PI3K/AKT signaling. KIF13A further interacts with Rab6 and the centralspindlin subunit MKLP1 to mediate midbody assembly during cytokinesis. Downstream outcomes include M6PR surface presentation, lysosomal enzyme secretion, and endosomal tubulation. The pathway features Arf1, AP-1, KIF13A, M6PR, and lysosomal hydrolases.
In the Jurkat T-cell model, KIF13A function is critical for immune-relevant processes. Endosomal recycling of the T-cell receptor and secretion of proteases such as cathepsins depend on efficient M6PR trafficking. Loss of KIF13A in these polyclonal knockout cells provides a platform to examine how disrupted M6PR transport alters lysosomal enzyme release and surface receptor dynamics in leukemia. Additionally, KIF13A??s role in cytokinesis makes this model useful for studying the link between intracellular transport, cell division, and cancer cell proliferation.
This knockout product supports applications including immunofluorescence and flow cytometry for M6PR expression, ELISA or enzymatic assays for cathepsin secretion, live-cell imaging of endosomal dynamics, and proliferation assays (MTS/MTT) to assess cytokinesis defects. It is suitable for high-content screening of T-cell trafficking modulators and as a validation tool in cancer immunotherapy research. For further technical details, please contact Ascent Research.
