The NHSL3 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte cell line. This gene-edited product provides a loss-of-function model for the NHSL3 gene, enabling systematic investigation of its roles in actin cytoskeletal organization and T cell biology. The polyclonal knockout pool preserves genetic diversity, avoiding clonal artifacts while allowing robust functional analyses in a human T cell context.
Jurkat cells are human T lymphoblastoid cells originally derived from an acute T cell leukemia patient. They serve as a well-characterized model for T cell receptor signaling, cytokine production, and immune response mechanisms. Their ease of culture and genetic tractability make them a cornerstone in immunological research. The Jurkat background is particularly suited for studying molecular events downstream of TCR engagement and integrin activation.
NHSL3 encodes an adaptor protein that scaffolds Abi1 and WAVE2 to activate the Arp2/3 complex, promoting branched actin polymerization essential for lamellipodia protrusion and directed cell migration. In T cells, this pathway is activated downstream of T cell receptor stimulation, chemokine receptors, and integrin engagement, linking extracellular cues to cytoskeletal rearrangement. NHSL3 interacts with core WAVE regulatory complex components including CYFIP1 and NCKAP1, and its function is regulated by the small GTPase Rac1. The resulting actin dynamics are critical for immune synapse formation and T cell activation, with downstream readouts such as phospho-Akt signaling and integrin-mediated adhesion.
Disruption of NHSL3 in Jurkat cells impairs the coordinated actin remodeling required for effective T cell migration and stable immunological synapse assembly, making this knockout model valuable for dissecting the molecular underpinnings of immune cell trafficking and activation. Because NHSL3-dependent lamellipodia formation also contributes to invasive migration, the model extends to cancer cell invasion studies, exploiting the leukemic origin of Jurkat cells to explore mechanisms of metastasis. The polyclonal format allows assessment of functional heterogeneity and avoids potential artifacts from single-cell cloning, while maintaining reliable CRISPR/Cas9-mediated gene disruption.
Researchers can employ this product in transwell migration assays to measure chemokine-driven movement, fluorescence microscopy to visualize F-actin organization, and flow cytometry to quantify T cell activation markers. Co-immunoprecipitation with Abi1 and western blotting for phospho-Akt provide direct biochemical readouts of pathway activity, and integrin adhesion assays reveal functional consequences of NHSL3 loss. These cells are thus suited for studies of actin cytoskeleton regulation, immune synapse dynamics, and the interplay between T cell receptor signaling and cell migration. For further details or technical support, please contact Ascent Research.
