PRMT2IP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line, providing a powerful loss-of-function model for investigating the role of PRMT2IP (methylosome protein 50, MEP50). This polyclonal population retains genetic heterogeneity, closely reflecting physiological variability, while enabling targeted disruption of the PRMT2IP gene via CRISPR/Cas9-mediated gene editing. Researchers can leverage these cells to study gene function without the artifacts associated with single-cell cloning, ensuring robust and reproducible experimental outcomes in downstream assays.
Jurkat cells are an immortalized human T lymphocyte line originally established from the peripheral blood of a 14-year-old male with acute T cell leukemia in 1976. Widely employed as a model system for T cell receptor (TCR) signaling, apoptosis, and HIV infection, Jurkat cells provide a physiologically relevant context for exploring the molecular underpinnings of T cell biology and leukemogenesis. Their ease of culture and well-characterized signaling networks make them an ideal host for CRISPR-based knockout studies, particularly for genes implicated in immune cell function and cancer.
PRMT2IP encodes MEP50, a WD40 repeat protein that functions as an obligate coactivator of protein arginine methyltransferase 5 (PRMT5). Together, PRMT5 and MEP50 form the methylosome, which catalyzes symmetric dimethylation of arginine residues on Sm proteins (SmB, SmD1, SmD3) and histones (H3R8, H4R3). This activity is essential for small nuclear ribonucleoprotein (snRNP) biogenesis and spliceosome assembly. PRMT2IP is regulated by upstream signals including TCR engagement, IL-2, PI3K, and AKT, and it directly interacts with PRMT5, pICln, RioK1, and the SMN complex. Downstream, it influences key molecules such as p53, E2F1, MYC, and CD44 splicing, thereby connecting arginine methylation to transcriptional control, cell cycle progression, and RNA processing.
In Jurkat T lymphocytes, knockout of PRMT2IP disrupts methylosome function, leading to impaired symmetric dimethylation of Sm proteins and subsequent defects in snRNP assembly. These splicing perturbations likely affect transcripts encoding critical TCR-proximal signaling components, including CD3, ZAP70, and LAT, as well as downstream effectors like PLC??1, NF-??B, and NFAT. Consequently, PRMT2IP-deficient cells may exhibit altered expression of activation markers (CD69, CD25), reduced proliferation, and enhanced apoptosis. This polyclonal knockout model thus offers a valuable system for dissecting how arginine methylation sculpts T cell responses and leukemic growth.
These PRMT2IP knockout polyclonal Jurkat cells are ideally suited for diverse research applications, including the study of TCR signaling, RNA splicing regulation, and methyltransferase inhibitor testing. Typical experimental workflows include Western blotting for symmetric dimethyl arginine (SDMA) marks, RT-qPCR for splicing isoform analysis, RNA-seq for transcriptome-wide splicing changes, flow cytometry for T cell activation markers, apoptosis assays (Annexin V/PI), MTS proliferation assays, and PRMT5 activity measurements. Moreover, this model supports CRISPR screening and drug discovery programs targeting PRMT5-dependent cancers. For further information or to inquire about custom cell engineering services, please contact Ascent Research.
