The ANKS3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte cell line. This product provides a pool of cells harboring targeted disruption of the ANKS3 gene, enabling loss-of-function studies in a heterogeneous knockout background. The polyclonal format preserves genetic diversity across edited alleles while abolishing ANKS3 protein expression, making it a versatile tool for investigating ciliary protein functions in an immune cell context.
Jurkat E6-1 cells are a well-established human T-cell leukemia line widely used for investigating T-cell signaling, apoptosis, and oncogenic transformation. As suspension-adapted immortalized lymphocytes, these cells express key T-cell surface markers and signaling machinery, facilitating biochemical and pharmacological analyses. The Jurkat model has been instrumental in elucidating pathways such as T-cell receptor (TCR) signaling, NF-??B activation, and IL-2 production, offering a robust platform for studying gene function in immune cell biology.
ANKS3 encodes a ciliary transition zone protein that scaffolds NPHP module components, including NPHP4, INVS (inversin), NEK8, and ANKS6, to regulate ciliogenesis and epithelial polarity. It operates downstream of ciliogenic transcription factors such as RFX3 and planar cell polarity cues, while its loss impairs ciliary transition zone assembly and disrupts downstream effectors like NEK8 kinase and inversin compartment complexes. ANKS3 is integral to pathways governing Wnt/planar cell polarity and Hippo signaling, and its dysfunction is linked to nephronophthisis, cystic kidney disease, and other ciliopathies.
Although lymphocytes are traditionally considered non-ciliated, emerging evidence indicates that immune cells, including T cells, can transiently assemble primary cilia under specific conditions, with implications for immune synapse organization and signal transduction. The ANKS3 knockout in Jurkat cells provides a unique model to dissect ciliary protein functions in T-lymphocyte biology and to explore how ciliopathy-associated proteins intersect with immune cell signaling. In the context of leukemia, deregulated Wnt and Hippo pathways contribute to malignant transformation, and this knockout enables systematic analysis of ANKS3??s role in these oncogenic networks.
Researchers can employ this knockout pool for co-immunoprecipitation assays to map ANKS3 interaction partners, immunofluorescence staining of ciliary markers to assess ciliation defects, and western blotting or RT-qPCR to quantify downstream signaling changes. Flow cytometry facilitates the detection of cilia-related antigens at the single-cell level, while functional assays can evaluate immune cell ciliation dynamics. This model is suitable for drug screening campaigns targeting cystic kidney disease and for mechanistic studies of ciliopathy-associated signaling in a tractable hematopoietic system. For additional technical details, please contact Ascent Research.
