The KIF2A Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with targeted disruption of the KIF2A gene in the Jurkat human T lymphocyte line. This heterogeneous knockout model abrogates KIF2A function without clonal selection, offering a physiologically relevant tool for loss-of-function studies.
Jurkat cells originate from a 14-year-old acute lymphoblastic leukemia patient and retain constitutive PI3K/Akt signaling due to defective PTEN and INPP5D. Their rapid proliferation and well-characterized T cell receptor signaling make them a standard model for T cell biology, leukemia, and mitosis research.
KIF2A is a kinesin-13 family member that depolymerizes microtubules by removing tubulin heterodimers from plus ends. It regulates mitotic spindle assembly, chromosome segregation, and microtubule network remodeling. KIF2A activity is controlled by Aurora A kinase, CDK1/cyclin B, and PLK1 phosphorylation, and is integrated with Wnt pathway components. It interacts with microtubules, tubulin, TIP150/EAF2, CENP-E, and APC to coordinate spindle dynamics. In neurons, KIF2A governs growth cone microtubule dynamics during migration and axon guidance, and its mutations underlie cortical dysplasia disorders. Its mitotic functions are conserved across cell types.
Within Jurkat cells, KIF2A is essential for accurate mitosis, and its disruption may reveal dependencies in leukemic contexts. The combination of KIF2A loss with hyperactive PI3K/Akt signaling provides a system to study how survival pathways intersect with mitotic regulation. This model enables comparison of KIF2A’s roles in T lymphocytes versus neural cells, aiding dissection of cell-type-specific functions.
Applications include target validation for KIF2A in cancer, screening of spindle-targeted chemotherapeutics, and mechanistic studies of microtubule dynamics. Assays such as Western blotting, immunofluorescence for spindle morphology, flow cytometry for cell cycle, RT-qPCR, and live-cell imaging of mitosis are directly applicable. The polyclonal knockout population is also suitable as a non-neuronal control for neurobiological KIF2A investigations. For further information, please contact Ascent Research.
