The KIF16B Knockout Jurkat Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes in which the KIF16B gene has been disrupted. This product provides a heterogeneous knockout model suitable for studying loss-of-function phenotypes without clonal selection biases. The polyclonal format preserves genetic diversity and facilitates the identification of robust, population-level effects across multiple independent editing events.
Derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia, the Jurkat cell line is a well-established model for T-cell receptor (TCR) signaling, apoptosis, and leukemogenesis. These suspension cells recapitulate key aspects of T-lymphocyte activation and are widely employed in immunological and cancer research. Their genetic tractability and responsiveness to exogenous stimuli make them ideal for interrogating the molecular machinery governing lymphocyte function and transformation.
KIF16B encodes a plus-end-directed kinesin-3 motor that binds phosphatidylinositol-3-phosphate (PI3P) on early endosomes via its PX domain and is recruited by the small GTPase Rab14. This motor complex drives transport of PI3P-enriched endosomes along microtubules toward the cell periphery, enabling rapid recycling of internalized cargo receptors, including epidermal growth factor receptor (EGFR), N-cadherin, and Frizzled. Through this mechanism, KIF16B sustains downstream ERK and AKT phosphorylation and regulates actomyosin contraction. The pathway is integral to endocytic recycling, receptor tyrosine kinase trafficking, and cell migration, with disruption leading to altered growth factor responsiveness and adhesion dynamics.
In the Jurkat T-cell context, KIF16B sits at the intersection of endosomal trafficking and receptor signaling pathways that govern T-cell activation, adhesion, and migration. Loss of KIF16B function may impair surface recycling of receptors critical for TCR signal maintenance and integrin-mediated adhesion, potentially attenuating PI3K/AKT and ERK cascades. Consequently, this knockout model provides unique insights into how endosome dynamics modulate T-cell responses, leukemia cell dissemination, and crosstalk between growth factor and immune signaling. It is particularly relevant for studying the role of endosomal motor proteins in hematological malignancy progression and immune synapse formation.
Typical research applications include detailed dissection of endosomal trafficking pathways, high-content screening for endocytosis modulators, quantitative analysis of receptor recycling kinetics, and functional migration and invasion assays. Investigators routinely employ Western blotting for phospho-ERK and phospho-AKT, flow cytometry to assess surface levels of EGFR or TCR subunits, and live-cell imaging to track endosome dynamics. Co-immunoprecipitation validates KIF16B-Rab14 interactions, and Transwell assays provide direct measures of cell migration. This tool is also suited for cancer metastasis and neurodevelopmental disorder studies. For further details and ordering information, please contact Ascent Research.
