This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat cells, a widely used human T lymphocyte line. The ARPC1A gene, encoding a critical subunit of the actin-related protein 2/3 (Arp2/3) complex, has been functionally disrupted through CRISPR/Cas9-mediated gene targeting, providing a genetically heterogeneous pool of cells with impaired ARPC1A expression. This format is ideal for studying loss-of-function effects in a population context, avoiding clonal artifacts and enabling robust, reproducible functional assays.
The Jurkat host cell line was originally established from the peripheral blood of a male patient with acute T cell leukemia. Jurkat cells are an immortalized T lymphocyte model that retains key features of T cell receptor (TCR) signaling, making them a cornerstone in immunology and cancer research. Their suspension growth and well-characterized signaling pathways facilitate high-throughput screening and detailed mechanistic studies, particularly in the contexts of T cell activation, leukemia biology, and actin cytoskeleton dynamics.
ARPC1A is an obligate component of the Arp2/3 complex, which nucleates branched actin filaments and is indispensable for processes requiring dynamic actin remodeling. The complex is activated downstream of the small GTPases Rac1 and Cdc42 through nucleation-promoting factors of the WAS/WAVE family, including WASP and WAVE2. Once activated, it interacts with actin and cortactin to drive lamellipodia formation, cell migration, endocytosis, and immune synapse assembly. In Jurkat cells, ARPC1A participates in TCR-stimulated actin polymerization, linking antigen recognition to T cell activation. Knockout therefore disrupts the Rac1/Cdc42-WAS/WAVE-Arp2/3-cortactin-F-actin cascade, impairing branched actin network formation.
In the Jurkat T lymphocyte context, ARPC1A disruption directly compromises actin-dependent processes essential for leukemic cell behavior. Loss of ARPC1A impairs chemotactic migration, reduces TCR microcluster formation, and alters immune synapse architecture, attenuating downstream signaling such as calcium flux and IL-2 production. This model recapitulates actin-related deficiencies observed in Wiskott-Aldrich syndrome and provides a platform to investigate the role of actin dynamics in T cell acute lymphoblastic leukemia (T-ALL) progression and metastasis. Functional validation can be performed using phalloidin staining to visualize F-actin, transwell migration assays to assess motility, and flow cytometry to measure activation markers.
Researchers can utilize this polyclonal knockout population to dissect T cell motility, immune synapse formation, and leukemic cell invasion. It is well suited for Western blotting and RT-qPCR to confirm target disruption, time-lapse imaging of actin dynamics, and drug screening campaigns aimed at identifying modulators of Arp2/3 complex function. Additional applications include co-culture systems to study T cell interactions and in vivo xenograft models to evaluate metastatic potential. For further technical specifications or ordering information, please contact Ascent Research.
