The IL27RA Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited pool of HAP1 cells carrying heterogeneous disruptions in the IL27RA gene. This polyclonal population eliminates IL27RA-mediated signaling across the pool, providing a convenient loss-of-function model for functional studies without clonal isolation. The knockout platform supports robust comparative analyses between wild?type and IL27RA?deficient cells.
HAP1 is a near-haploid human cell line derived from chronic myeloid leukemia with a fibroblast-like morphology. Its haploid karyotype allows for unambiguous gene editing, as a single allele is targeted, yielding complete functional knockout in the edited population. HAP1 is widely adopted for genetic screens, signaling assays, and drug target validation due to its stable growth and well-characterized molecular background.
IL27RA encodes the alpha subunit of the interleukin?27 receptor, which pairs with gp130 (IL6ST) to transduce IL27 signals. Ligand binding activates associated JAK1, JAK2, and TYK2 kinases, leading to phosphorylation of STAT1 and STAT3 transcription factors. These in turn regulate targets such as T?bet, IL?10, and SOCS3, linking IL27 to Th1 differentiation and anti?inflammatory feedback. Upstream regulators include IL27 and type I interferons. The knockout therefore specifically blocks IL27-induced JAK/STAT cascade.
In the HAP1 background, the IL27RA knockout provides a simplified system to dissect JAK/STAT signaling without interference from adaptive immune receptors. The haploid nature ensures a clean genotype-phenotype relationship, making the pool ideal for dose?response studies, phospho?STAT immunoblotting, and transcriptomic profiling. The polyclonal format further mitigates clonal bias, offering a representative model for high?throughput screening applications.
This knockout population is applicable to cancer immunotherapy research, autoimmune disease modeling, and cytokine network analysis. Representative assays include phospho?STAT1/STAT3 western blot, quantitative RT?PCR for IL?10, flow?cytometric assessment of signaling intermediates, and RNA?seq for global expression changes. By removing IL27RA, researchers can distinguish IL27?driven effects from overlapping signals in inflammation and oncology pathways. For additional information or custom requests, please contact Ascent Research.
