The ACTN1 Knockout Jurkat Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of Jurkat cells carrying targeted disruption of the ACTN1 gene. This loss-of-function model is generated in an immortalized human T lymphocyte line and is supplied as a mixed polyclonal pool, enabling robust experimental analysis of alpha-actinin-1 function without the clonal variability of single-cell-derived lines. The polyclonal format preserves genetic heterogeneity while ensuring effective gene knockout across the cell population, making it suitable for functional studies that require reproducible and scalable cell material.
Jurkat cells are a well-established model originating from a patient with T cell acute lymphoblastic leukemia (T-ALL). They harbor important oncogenic mutations, including alterations in PTEN and p53, and are widely used to study T cell receptor (TCR) signaling, leukemogenesis, and immune cell biology. The Jurkat background provides a genetically defined, high-proliferation human T lymphocyte system in which actin cytoskeleton dynamics and adhesion can be interrogated in the context of malignant transformation and T cell activation.
ACTN1 encodes alpha-actinin-1, an actin-crosslinking protein that anchors filamentous actin to focal adhesion complexes through interactions with integrins (such as ITGB1), vinculin, and zyxin. It acts as a key scaffold in mechanotransduction pathways, regulated by mechanical tension, integrin activation, and growth factors such as TGFB1 and EGF, and functions downstream of transcriptional regulators SRF and MRTF-A within focal adhesion and integrin signaling networks. ACTN1 drives actin cytoskeleton reorganization, focal adhesion maturation, and recruitment of vinculin, zyxin, and paxillin to adhesion complexes, leading to FAK activation. Through interactions with ICAM1 and LPP, alpha-actinin-1 integrates cell adhesion and migration. Its disruption thus impairs cytoskeletal linkage to the extracellular matrix.
In Jurkat T lymphocytes, ACTN1 knockout disrupts the cortical actin network and dynamic reorganization required for T cell migration, adhesion, and immunological synapse formation. Since Jurkat cells are used to model T-ALL and TCR signaling, loss of alpha-actinin-1 provides a tool to dissect how cytoskeletal defects influence leukemic cell adhesion and invasive potential, as well as the spatial organization of signaling molecules during T cell activation. Furthermore, ACTN1 mutations are linked to congenital macrothrombocytopenia, and although Jurkat cells are not platelets, the model allows functional dissection of alpha-actinin-1-dependent cytoskeletal pathways relevant to platelet production and function in a genetically manipulable system.
Applications include investigations of cancer cell migration, invasion, and metastasis; studies of cytoskeletal dynamics during T cell activation; and analysis of focal adhesion turnover. It may be employed in adhesion and migration assays (e.g., Boyden chamber), immunofluorescence microscopy for actin and focal adhesion markers, flow cytometry for integrin surface expression, and phospho-specific flow cytometry to evaluate TCR-proximal signaling. Drug screening targeting adhesion-dependent processes or cytoskeletal regulators can also leverage this model. For additional information or technical support, please contact Ascent Research.
