The ANKRD10 Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line, engineered to disrupt the ANKRD10 gene. This loss-of-function model enables investigation of the gene??s role in cellular processes without the confounding influence of clonal selection. The polyclonal format captures a heterogeneous mix of knockout variants, allowing functional studies that reflect diverse editing outcomes while maintaining overall target-gene disruption. These cells are supplied as a ready-to-use suspension culture suitable for a broad range of downstream assays in T-cell biology and signaling research.
The parental Jurkat cell line is an immortalized human T lymphocyte clone (E6-1) originally established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Jurkat cells are widely adopted in biomedical research for studying T-cell receptor (TCR) signaling, apoptosis, HIV infection, and T-cell activation due to their robust growth and well-characterized signaling machinery. The line provides a physiologically relevant context for examining the function of adaptor and scaffold proteins in lymphocyte signaling networks.
ANKRD10 encodes a member of the ankyrin repeat domain-containing protein family, predicted to function as a scaffold or adaptor mediating protein?Cprotein interactions. Through its ankyrin repeat motifs, the protein likely assembles multi-protein complexes and integrates into signal transduction and cytoskeletal organization pathways. In T cells, ANKRD10 may be regulated downstream of TCR activation, although its precise upstream regulators remain undefined. The protein is proposed to interact with cytoskeletal components such as actin and spectrin, as well as with signaling adaptors and transcription factors, forming complexes that could influence pathway dynamics.
In the Jurkat cell background, ANKRD10 knockout provides a powerful model to explore the protein??s contribution to TCR-proximal signaling events and cytoskeletal remodeling. The polyclonal population avoids potential artifacts arising from monoclonal isolation, thus offering a more representative system for functional genomics studies. Since ANKRD10??s interactors and downstream targets are not characterized, this model serves as a discovery platform for identifying novel protein partners and for mapping the signaling modules dependent on ankyrin repeat-mediated scaffolding.
Key applications include quantitative analysis of gene expression via RT-qPCR, protein-level validation by Western blotting and immunofluorescence, and functional assays using flow cytometry to monitor T-cell activation markers (e.g., CD69, IL-2). Phospho-signaling profiling through TCR pathway components (such as ZAP-70, LAT, and ERK) and co-immunoprecipitation experiments to identify interactors are highly compatible with this system. Additionally, apoptosis and proliferation assays can elucidate the consequences of ANKRD10 loss. This knockout model is ideally suited for investigators interrogating scaffold protein functions in T-cell biology, leukemia, and protein interaction networks. For more information, please contact Ascent Research.
