The ARPC1B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte line, designed to disrupt target-gene expression of ARPC1B. This product provides a loss-of-function model to investigate the p41 subunit of the actin-related protein 2/3 (Arp2/3) complex, a central nucleator of branched actin filaments. The polyclonal format preserves the heterogeneous genetic background inherent to CRISPR-mediated gene disruption, enabling robust population-level studies without clonal selection artifacts. Researchers can utilize these cells to dissect actin-dependent processes critical for T-cell biology and immune function.
The Jurkat host cell line is an immortalized human T-lymphocyte model originally established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Jurkat cells are extensively characterized for studying T-cell receptor signaling, activation, and apoptosis, offering a tractable system to examine the molecular events governing immune cell responses. Their suspension growth properties and well-defined signaling cascades make them especially suitable for CRISPR-based genetic manipulation, allowing direct interrogation of cytoskeletal dynamics in a physiologically relevant lymphoid context without the need for primary cell isolation. ARPC1B encodes the p41 subunit of the heptameric Arp2/3 complex, which is activated downstream of the Rho-family GTPases CDC42 and RAC1 via nucleation-promoting factors such as WASL/N-WASP.
Upon activation, the complex interacts with actin monomers to generate branched filament networks, driving processes like lamellipodial protrusion, endocytic vesicle scission, and phagocytic cup formation. The ARPC1B subunit is integral to complex stability and function, forming direct interactions with ARPC2, ARPC3, ARPC4, ARPC5, ACTR2, and ACTR3, as well as regulatory proteins including WIPF1, cortactin, and coronin. This signaling network is tightly regulated by upstream inputs from PIP2 and the WAS complex, linking extracellular cues to dynamic actin reorganization. In the Jurkat T-cell context, ARPC1B-mediated actin nucleation is essential for the formation and stabilization of the immunological synapse, a structured interface between T cells and antigen-presenting cells that orchestrates sustained signaling.
Disruption of ARPC1B impairs synapse architecture, reducing T-cell activation and cytokine production, and also compromises integrin-dependent adhesion and transendothelial migration. These defects mirror the clinical phenotype of ARPC1B deficiency, a combined immunodeficiency characterized by immune dysregulation, allergy, autoinflammation, and platelet abnormalities. Thus, this knockout model recapitulates key aspects of leukocyte adhesion deficiency variants and actinopathies, offering a platform to study disease mechanisms. The ARPC1B Knockout Jurkat Polyclonal Cells support a wide range of research applications, including mechanistic studies of actin cytoskeleton dynamics during T-cell activation, migration, and endocytosis.
Typical assays involve Western blotting to confirm protein loss, immunofluorescence with phalloidin to visualize F-actin architecture, flow cytometry for surface receptor and activation marker analysis, and functional tests such as transwell migration, immune synapse formation assays, and cell adhesion measurements. The model is also amenable to biochemical techniques like co-immunoprecipitation of Arp2/3 complex components and pyrene actin polymerization assays. Additionally, these cells enable drug screening for modulators of cytoskeletal pathways and interrogation of signaling networks involving CDC42, RAC1, and Wiskott-Aldrich syndrome protein. For further information, please contact Ascent Research.
