The BAIAP2L1 Knockout Jurkat Polyclonal Cells are a genetically modified human T lymphocyte population generated via CRISPR/Cas9-mediated disruption of the BAIAP2L1 gene locus. This polyclonal knockout pool enables loss-of-function studies in an immortalized T-cell background, providing a versatile model for investigating the BAIAP2L1 adaptor protein in diverse signaling contexts.
The Jurkat cell line was originally derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia and has become a widely used model for T-cell signaling, apoptosis, and cancer biology. These cells express key components of the T-cell receptor signaling machinery and retain responsiveness to phorbol esters and other stimuli. The Jurkat host provides a reproducible, well-characterized system amenable to transfection, live-cell imaging, and migration assays.
BAIAP2L1 (also known as IRTKS) functions as a membrane curvature-sensing adaptor that physically couples activated receptor tyrosine kinases, including the insulin receptor and EGFR, to actin cytoskeletal remodeling. Through its I-BAR domain, BAIAP2L1 recognizes and stabilizes negative membrane curvature, promoting filopodia initiation. Upon phosphorylation by upstream kinases such as SRC and PI3K, BAIAP2L1 recruits and activates downstream effectors, particularly the small GTPase RAC1. BAIAP2L1 directly interacts with IRS4, ENAH, BAIAP2 (IRSp53), and CDC42, forming complexes that orchestrate signal-dependent actin polymerization. The RAC1?CWAVE?CARP2/3 cascade, along with cortactin, drives branched actin nucleation at the plasma membrane, facilitating cell migration and morphological change.
In the Jurkat T-lymphocyte context, disruption of BAIAP2L1 enables dissection of its role in leukocyte migration, immune synapse formation, and leukemia cell invasiveness. Given that BAIAP2L1 has been implicated in colorectal and gastric cancer progression, this knockout model also supports comparative studies of solid tumor versus hematological malignancy cell migration mechanisms. The Jurkat polyclonal population offers a heterogeneous genetic background that better reflects the natural variability seen in tumor populations compared to single-cell clones, without the need for clonal selection.
Researchers can employ these BAIAP2L1 Knockout Jurkat Polyclonal Cells in transwell migration assays, immunofluorescence staining for filopodia markers, and RAC1 GTPase activation assays to dissect the BAIAP2L1-dependent signaling axis. Western blotting and co-immunoprecipitation experiments can validate altered expression and protein interactions, while phospho-signaling analyses monitor insulin receptor and EGFR pathway activity. This model is well suited for investigations into insulin receptor signaling dynamics, T-cell motility, and the identification of BAIAP2L1 interaction partners. For additional technical specifications or ordering information, please contact Ascent Research.
