ATP1B1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat T lymphocytes, engineered to disrupt the ATP1B1 gene and serve as a loss-of-function model for the beta-1 subunit of Na+/K+-ATPase. This knockout product format provides a heterogeneous population of edited cells, enabling robust assessment of gene function without clonal isolation artifacts.
The Jurkat host cell line is a widely used model of acute T cell leukemia, originating from a 14-year-old male patient. These suspension-adapted T lymphoblastoid cells are extensively employed to investigate T cell receptor signaling, apoptosis, and leukemogenesis. Their well-characterized signaling networks and ease of genetic manipulation make them an ideal platform for ion transporter studies in a lymphoid context.
ATP1B1 encodes the essential beta-1 subunit of the Na+/K+-ATPase, which assembles with the alpha-1 catalytic subunit (ATP1A1) to form the active ion pump. This pump is transcriptionally regulated by thyroid hormone, aldosterone, Sp1, and CREB, and interacts with ankyrin, Src kinase, and FXYD1 (phospholemman). Knockout of ATP1B1 disrupts electrogenic Na+ and K+ transport, compromising membrane potential maintenance, cell volume regulation, and calcium handling via the Na+/Ca2+ exchanger. Importantly, the Na+/K+-ATPase also functions as a signaling scaffold, activating Src kinase to initiate downstream MAPK and PI3K/Akt cascades. Thus, loss of the beta-1 subunit not only impairs ion homeostasis but also attenuates Src-mediated signal transduction.
In Jurkat T lymphocytes, ATP1B1 disruption has pronounced functional consequences. Impaired Na+/K+-ATPase activity alters the resting membrane potential and intracellular ion concentrations, which can affect T cell antigen receptor (TCR)-induced calcium flux and downstream gene expression. This model enables investigation of how electrochemical gradients modulate immune cell activation, proliferation, and leukemic cell survival. Given the Na+/K+-ATPase??s role in Src kinase activation, the knockout may also uncover contributions to TCR signaling pathways that require Src-family kinases. Consequently, these polyclonal knockout cells provide a physiologically relevant system to dissect ion transport-dependent signaling in malignant T cells.
Researchers can employ ATP1B1 Knockout Jurkat Polyclonal Cells in diverse experimental contexts. Western blotting and activity assays confirm loss of beta-1 expression and pump function, while flow cytometry allows monitoring of cell size, viability, and surface activation markers. Functional studies using fluorescent dyes like DiBAC4(3) measure membrane potential changes, and ion-sensitive probes quantify intracellular Na+ and K+ levels. TCR stimulation with CD3/CD28 antibodies permits analysis of activation-induced signaling, and proliferation assays assess growth defects. Additionally, these cells facilitate drug screening for cardiac glycosides and other pump modulators in a T cell setting. Transcriptomic approaches such as RNA-seq can reveal global gene expression changes resulting from ATP1B1 loss. For more information or to request a quote, please contact Ascent Research.
