BCAR1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the BCAR1 gene has been disrupted to ablate expression of the p130Cas scaffold protein. Generated in the Jurkat T lymphoblastoid line, this loss-of-function model provides a heterogeneous knockout pool ideal for studies of integrin-mediated signaling without clonal selection artifacts.
The Jurkat cell line, derived from a 14-year-old acute T-cell leukemia patient, is a classic model for T-lymphocyte signal transduction and apoptosis. Although suspension-adapted, these cells express functional integrins and downstream effectors, enabling dissection of focal adhesion signaling in an immune context. The parental line??s intact SRC/FAK machinery makes it well-suited for investigating BCAR1-dependent pathways.
BCAR1 (p130Cas) is a critical scaffold protein that transduces integrin-mediated signals. Upon integrin binding to extracellular matrix ligands, BCAR1 becomes tyrosine-phosphorylated by SRC-family kinases and FAK at multiple YxxP motifs. This creates high-affinity binding sites for the adaptor proteins Crk and Nck, which in turn recruit the DOCK180 guanine nucleotide exchange factor to activate Rac. Rac triggers actin polymerization and lamellipodium formation, driving cell migration. Simultaneously, BCAR1 engagement promotes PI3K/AKT and MAPK/ERK cascades, fostering survival and proliferation. BCAR1 also interacts with focal adhesion components paxillin, vinculin, and talin, linking integrin clusters to the cytoskeleton. Upstream, integrin ??/?? heterodimers, growth factor receptors (EGFR, HER2), and SRC kinases converge on BCAR1, while downstream effectors include paxillin, Src, Crk, ERK, AKT, and Rac, underscoring its role as a nexus for adhesion and growth factor signaling.
In Jurkat T lymphoblastoid cells, BCAR1 knockout allows detailed investigation of integrin signaling in a leukemic T-cell context. This model is valuable for studying how BCAR1 facilitates T-cell adhesion, chemotaxis, and transendothelial migration??processes crucial for immune surveillance and leukemic dissemination. Moreover, the knockout cells help elucidate BCAR1??s role in cancer metastasis and chemoresistance, as BCAR1 overexpression is linked to poor prognosis in solid tumors and hematologic malignancies. By comparing knockout and wild-type Jurkat cells, researchers can identify BCAR1-dependent signaling nodes required for T-cell activation and survival, and screen for inhibitors that block BCAR1-mediated pro-metastatic pathways.
These polyclonal knockout cells are ideal for western blotting of BCAR1 and phospho-BCAR1 after integrin stimulation, co-immunoprecipitation of BCAR1 with Crk, FAK, or Src, and quantitative adhesion assays on fibronectin- or ICAM-1-coated plates. Migration and invasion can be assessed in transwell chambers, and flow cytometry used to monitor surface integrin activation. Phospho-kinase arrays enable profiling of downstream AKT and ERK pathways. Additionally, the knockout model supports high-throughput drug screening for anti-metastatic compounds and T-cell adhesion modulators. For technical support or additional information, please contact Ascent Research.
