The HNRNPAB Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the HNRNPAB gene in the Jurkat human T lymphocyte cell line. This loss-of-function model enables investigation of HNRNPAB-dependent post-transcriptional regulatory mechanisms without selection for a single clonal genotype, preserving the heterogeneity of polyclonal editing. The edited pool facilitates functional studies where broad gene disruption is sufficient to elicit measurable biological effects.
Jurkat cells are an immortalized T lymphocyte line derived from peripheral blood of a 14-year-old male with acute T-cell leukemia. These suspension cells are a well-established model for T-cell receptor (TCR) signaling, apoptosis, and HIV infection, offering rapid proliferation and defined signaling pathways suitable for gene knockout studies. Their robust growth and extensively characterized signaling networks make them an ideal host for examining RNA-binding proteins in immune regulation.
HNRNPAB encodes a heterogeneous nuclear ribonucleoprotein that preferentially binds A/U-rich sequences. It regulates alternative splicing, mRNA transport, and translational control, interacting with key splicing factors U2AF and serine/arginine-rich (SR) proteins, and associating with RNA polymerase II and nuclear transport receptors. Upstream inputs include transcriptional regulation by c-Myc and T-cell receptor stimulation, as well as post-translational phosphorylation. Downstream, HNRNPAB modulates splicing and stability of immune-related transcripts containing AU-rich elements, functioning alongside U1 snRNP, U2 snRNP, HNRNPA1, HNRNPA2B1, and mRNA export receptors.
Disruption of HNRNPAB in Jurkat cells ablates critical post-transcriptional checkpoints, altering the expression of genes governing TCR signaling and apoptosis. This knockout model is highly relevant for investigating how aberrant RNA processing contributes to T-cell leukemia, lymphomas, and splicing-related diseases such as amyotrophic lateral sclerosis. The polyclonal format enables unbiased assessment of population-level phenotypic changes.
Researchers can apply these cells to functional genomics of RNA-binding proteins, alternative splicing analyses in leukemia, and drug target discovery. Compatible assays include Western blotting, RT-qPCR for splice variants, RNA immunoprecipitation, RNA-seq, flow cytometry for apoptosis and T-cell activation, and migration/invasion studies. For technical inquiries, contact Ascent Research.
