PRMT2IP Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population featuring targeted disruption of the PRMT2IP gene in the near-haploid HAP1 human cell line. This loss-of-function model eliminates PRMT2IP protein expression, facilitating study of its role in transcriptional coactivation and arginine methylation-dependent signaling. The polyclonal format provides a heterogeneous pool of edited cells suitable for pooled screens or bulk biochemical analyses.
HAP1 cells are derived from the male KBM-7 chronic myeloid leukemia line, exhibit a fibroblast-like morphology, and are near-haploid for most chromosomes. This haploid state simplifies genetic analysis by avoiding functional redundancy from a second allele, making HAP1 an optimal host for generating clean CRISPR knockout models and for high-throughput genetic screens.
PRMT2IP interacts with protein arginine methyltransferase 2 (PRMT2), a coactivator for Wnt and nuclear hormone receptor pathways. The complex is recruited by transcription factors such as CTNNB1/TCF/LEF downstream of Wnt ligands, or by ESR1 in response to estrogen, and promotes arginine methylation of histones to enhance chromatin accessibility and target gene transcription, including CCND1 (cyclin D1). Thus, PRMT2IP links hormonal and Wnt signals to epigenetic regulation and proliferation.
In HAP1 cells, PRMT2IP knockout disrupts the PRMT2 coactivator complex, likely impairing histone methylation and downstream gene expression programs. The haploid background ensures a pure genetic context, allowing direct comparison of wild-type and knockout populations to assess the dependency of Wnt- or hormone-driven transcription on PRMT2IP.
Applications encompass co-immunoprecipitation for protein interaction studies, luciferase reporter assays for pathway activity, ChIP-qPCR for histone methylation monitoring, RT-qPCR for target gene analysis, and Western blotting. These tools are valuable for dissecting PRMT2 signaling, exploring hormone-dependent cancer mechanisms, and screening for PRMT2IP-PRMT2 modulators. For further information, contact Ascent Research.