The KIF3B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T lymphocyte line. This product targets the KIF3B gene, creating a loss-of-function model to investigate kinesin-2 motor subunit biology. The polyclonal format provides a heterogeneous pool of gene-disrupted cells, suitable for pooled functional studies and signaling analyses without single-cell cloning. Cells are supplied ready for use in advanced biomedical research applications.
Jurkat cells, isolated from a 14-year-old male with acute T cell leukemia, serve as a standard model for T cell signaling, apoptosis, and leukemia research. These cells express T cell receptors and respond to stimuli such as PMA/ionomycin, enabling interrogation of TCR pathways, cytokine production, and cell death mechanisms. The Jurkat background thus provides a well-characterized, manipulable host for studying gene function in lymphocyte biology and oncogenic transformation.
KIF3B encodes a motor subunit of heterotrimeric kinesin-2, which partners with KIF3A and KAP3 to drive anterograde microtubule-based transport. This complex is critical for intraflagellar transport, ciliogenesis, and non-ciliary trafficking that modulates Hedgehog and Wnt signaling. KIF3B expression is regulated by RFX transcription factors, and its activity is modified by Aurora A kinase. The motor interacts with IFT-B components (IFT88, IFT172), dynein, and the BBSome to deliver signaling molecules. Disruption of KIF3B impairs GLI transcription factor processing in the Hedgehog pathway (via SMO, PTCH1, SUFU) and alters ??-catenin localization in Wnt signaling (through DVL, APC, AXIN), thereby linking microtubule-based transport to developmental and disease-associated cascades.
In Jurkat T cells, KIF3B knockout disrupts anterograde trafficking, potentially derailing Hedgehog and Wnt pathway functions relevant to T cell activation, proliferation, and apoptosis. Although Jurkat cells lack cilia, kinesin-2 performs essential non-ciliary roles in immune synapse formation and polarized transport, making this model valuable for dissecting kinesin-dependent processes in lymphocyte biology and leukemia. The knockout pool enables investigation of how trafficking defects influence signaling dysregulation in a leukemic context.
Research uses include examining kinesin-2 functions in TCR signaling, cytokine secretion, and immune synapse dynamics, as well as studying Hedgehog/Wnt pathway involvement in leukemia. Representative assays comprise Western blotting for GLI and ??-catenin, RT-qPCR for target genes, immunofluorescence for protein localization, flow cytometry for apoptosis (Annexin V) and surface markers, and proliferation assays (MTT/XTT). Phospho-protein analysis further maps signaling alterations. This polyclonal knockout system supports functional genomics and signal transduction research. For further information, contact Ascent Research.
