The ITGA2 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with targeted disruption of the ITGA2 gene. This knockout model eliminates expression of the integrin alpha 2 subunit, providing a loss-of-function tool for studying integrin-mediated adhesion and signaling. As a polyclonal pool, it avoids clonal artifacts and better represents heterogeneous gene-editing outcomes, suitable for population-based functional analyses.
Jurkat cells are an immortalized human T lymphocyte line derived from acute T cell leukemia. They serve as a widely used model for adaptive immune responses, including T cell receptor signaling, cytokine production, and activation. Their robust proliferation and defined integrin profile make them an ideal host for dissecting ITGA2 function in contexts such as leukocyte adhesion, transendothelial migration, and leukemia cell biology.
ITGA2 encodes the alpha 2 integrin subunit, which pairs with ITGB1 (integrin beta 1) to form the collagen receptor VLA-2. Ligand binding activates focal adhesion kinase (FAK) and Src, which in turn phosphorylate downstream targets like paxillin and regulate Rho GTPases (RhoA, Rac1). This cascade triggers MAPK/ERK and PI3K/Akt signaling, controlling adhesion, migration, and survival. Upstream, ITGA2 is regulated by collagen binding and inside-out signaling through talin and kindlin, as well as by cytokines such as TGF-beta, IL-1, and TNF. Interacting proteins include vinculin and the actin cytoskeleton.
In Jurkat cells, loss of ITGA2 disrupts collagen-dependent adhesion and downstream signaling, affecting processes like transendothelial migration and T cell activation. This polyclonal knockout model is valuable for exploring how integrin signals intersect with immune responses and contribute to diseases such as T cell leukemia metastasis, thrombosis, and chronic inflammation. The mixed genotype avoids clone-specific biases, offering a robust platform for reproducible functional studies.
Applications include flow cytometric verification of ITGA2 surface loss, collagen-based adhesion assays, and western blotting for phospho-FAK and phospho-Akt. Migration/invasion assays, immunofluorescence for focal adhesion components (e.g., paxillin), and co-immunoprecipitation of ITGB1 enable detailed mechanistic studies. These cells are suitable for drug screening targeting integrin-dependent pathways and for transcriptomic analyses via RNA-seq. For inquiries, contact Ascent Research.
