The BROX Knockout Jurkat Polyclonal Cells product from Ascent Research provides a CRISPR/Cas9-edited polyclonal cell population derived from the Jurkat T lymphocyte line, featuring targeted disruption of the BROX gene. This knockout model enables loss-of-function studies of BROX without monoclonal selection, representing a heterogeneous pool of edited cells useful for investigating endosomal sorting and receptor degradation pathways. The polyclonal format maintains genetic diversity while ensuring broad gene disruption, suitable for applications requiring robust population-level phenotypes.
Jurkat cells are an immortalized human T lymphocyte line originally isolated from the peripheral blood of a 14-year-old male with acute T cell leukemia. Widely used as a model system for T cell signaling, activation, and leukemia biology, these suspension cells express key T cell receptors and downstream signaling components. Their transformed phenotype and ease of culture make them ideal for CRISPR-based genome editing and functional genomics studies in the context of hematological malignancies and immune cell regulation.
BROX encodes an endosomal sorting protein containing a BRO1 domain and a CAAX prenylation motif, functioning as an adaptor in the ESCRT pathway. It associates with HD-PTP (PTPN23) and the ESCRT-III component CHMP4B to direct ubiquitinated cargo, including activated EGFR and PDGFR, into intraluminal vesicles of multivesicular bodies for lysosomal degradation. Upstream, receptor tyrosine kinase activation and ubiquitination drive BROX-mediated sorting; downstream, this process controls signal attenuation by targeting receptors for destruction in the lysosome, thereby regulating the intensity and duration of signaling cascades.
In Jurkat T cells, BROX knockout disrupts the endosomal sorting machinery, leading to impaired degradation of ubiquitinated receptors and altered signaling dynamics. This perturbation is particularly relevant for understanding T cell activation, where receptor tyrosine kinases and immune receptors undergo ligand-induced downregulation. Given the origin of Jurkat cells from acute T cell leukemia, the BROX knockout also provides a platform to explore how defective endosomal trafficking contributes to oncogenic signaling, potentially revealing vulnerabilities in leukemic T cells or identifying trafficking modulators as therapeutic targets.
Researchers can employ these polyclonal BROX knockout cells in diverse experimental workflows, including Western blotting to monitor EGFR degradation kinetics, flow cytometry to quantify surface receptor retention, and co-immunoprecipitation to assess interactions with HD-PTP or ESCRT-III components. Additional applications encompass immunofluorescence colocalization studies, lysosomal inhibition experiments with chloroquine, and transcriptomic profiling via RNA-seq to capture global gene expression changes. This product is especially suited for drug screening campaigns focused on endocytic trafficking modulators and functional dissection of the ESCRT pathway in T cell leukemia. For technical inquiries or custom cell engineering requests, please contact Ascent Research.
