ITGA5 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte leukemia cell line. This loss-of-function model targets the ITGA5 gene, encoding integrin alpha-5. The polyclonal nature retains heterogeneity, avoiding clonal artifacts. CRISPR/Cas9-mediated gene disruption provides a robust knockout tool for functional studies.
The Jurkat host is an immortalized CD4+ T-cell line from a 14-year-old male with acute T-cell leukemia. Jurkat cells are widely used to study T-cell receptor signaling, cytokine production, and leukemia biology. Their suspension growth and well-characterized signal transduction make them suitable for high-throughput screening and molecular analysis.
ITGA5 encodes integrin alpha-5, which heterodimerizes with integrin beta-1 (ITGB1) to form the fibronectin receptor. Upon fibronectin binding, the ITGA5?CITGB1 complex recruits focal adhesion kinase (FAK) and Src, activating PI3K-Akt and MAPK/ERK pathways. Downstream effectors include Rho GTPases (RhoA, Rac1) that regulate cytoskeletal dynamics, promoting adhesion, migration, proliferation, and survival. Upstream regulators include EGF, TGF-beta, and TNF-alpha, while adaptors talin, vinculin, and paxillin link the receptor to actin. ITGA5 is a central mechanotransduction node.
In Jurkat T leukemia cells, ITGA5 mediates adhesive and migratory functions relevant to tissue infiltration and immune synapse formation. Disrupting ITGA5 allows dissection of integrin-specific signaling from TCR-mediated pathways. Since PI3K-Akt and MAPK cascades are commonly dysregulated in leukemia, this knockout model enables study of fibronectin receptor contributions to oncogenic signaling. The polyclonal pool also permits analysis of functional heterogeneity in adhesion responses.
Applications include cell adhesion assays on fibronectin, transwell migration/invasion studies, and phospho-signaling analysis via western blotting or flow cytometry. The cells support research on cancer metastasis, angiogenesis, fibrosis, and drug resistance. They are also valuable for investigating integrin roles in T-cell trafficking and activation. For additional details, contact Ascent Research.
