The HNRNPLL Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal population derived from the Jurkat human T lymphocyte cell line. This product consists of a heterogeneous pool of cells carrying targeted disruptions in the HNRNPLL gene, creating a functional knockout model for investigating RNA-binding protein-mediated regulation of alternative splicing. The polyclonal format provides a loss-of-function system without clonal selection, enabling studies of gene function in a mixed-edited population that reflects the complexity of endogenous gene disruption.
Jurkat cells are an immortalized CD4+ T lymphocyte line originally isolated from the peripheral blood of a 14-year-old male with acute T cell leukemia. This cell line serves as a classic model for T cell signaling, activation, and apoptosis, extensively employed in immunological and cancer research. Its leukemic origin retains key features of T cell receptor (TCR) signaling machinery, making it particularly suitable for dissecting molecular events in T cell biology and leukemia pathophysiology.
HNRNPLL encodes a heterogeneous nuclear ribonucleoprotein that functions as a splicing regulator, with a critical role in modulating CD45 (PTPRC) pre-mRNA processing. In response to T cell receptor engagement, HNRNPLL binds to CD45 pre-mRNA and interacts with spliceosome components including U2AF and SR proteins to promote inclusion of exon 4, thereby increasing the CD45RA isoform. This isoform switch enhances proximal TCR signaling: CD45RA dephosphorylates regulatory tyrosines of Src family kinases LCK and FYN, facilitating their activation and downstream phosphorylation of ZAP70, linker for activation of T cells (LAT), and nuclear factor of activated T cells (NFAT). Consequently, HNRNPLL lowers the threshold for T cell activation and shapes the magnitude of adaptive immune responses.
In the Jurkat cellular context, disruption of HNRNPLL perturbs CD45 isoform balance, leading to altered TCR signal strength and downstream gene expression. This knockout model enables precise dissection of HNRNPLL-dependent splicing events and their impact on leukemic T cell behavior. Given the role of CD45 isoforms in autoimmune disorders and immunodeficiency, the cells provide a relevant platform for exploring how aberrant alternative splicing contributes to immune dysregulation and tumorigenesis. Moreover, the Jurkat background bridges mechanisms of normal T cell activation with malignant transformation, offering insights into T cell leukemia pathogenesis.
Researchers can employ this polyclonal knockout product in a broad array of applications, including analyses of alternative splicing by RNA-seq or RT-PCR, quantitative assessment of CD45RA and CD45RO isoforms via western blotting and flow cytometry, and functional studies of TCR signaling using calcium flux assays, cytokine ELISA, and phospho-immunoblotting for ZAP70 and LCK activation. The model is also valuable for drug screening campaigns aimed at identifying modulators of T cell activation or splicing. For additional information, technical support, or custom requirements, please contact Ascent Research.
