The IL11 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human IL11 gene. This loss-of-function model is produced in HAP1 cells, a near-haploid human cell line favored for genetic screening and functional genomics. The polyclonal format provides a heterogeneous pool of gene-disrupted cells, avoiding clonal bias. This product enables investigation of IL-11-dependent pathways without the need for single-cell cloning.
HAP1 is a near-haploid cell line derived from the KBM-7 chronic myelogenous leukemia (CML) line. It retains a stable haploid karyotype except for disomy of chromosome 8, which simplifies loss-of-function studies by reducing gene copy number to one in most loci. HAP1 cells maintain key signaling pathways, including cytokine-responsive JAK/STAT and MAPK cascades, and are widely used in CRISPR-based functional genomics and drug discovery.
IL-11 is a pleiotropic IL-6 family cytokine that signals via a receptor complex of IL11RA and gp130 (IL6ST). Ligand binding triggers activation of JAK1 and TYK2 kinases, phosphorylation of STAT3, and induction of target genes such as SOCS3, BCL-2, MMP9, fibronectin, and collagen. Parallel activation of MAPK/ERK and PI3K/Akt pathways promotes survival, proliferation, and matrix remodeling. IL-11 expression is transcriptionally regulated by TGF-??1, IL-1??, TNF-??, AP-1, and SMAD3, embedding it in fibrotic and inflammatory signaling networks.
The near-haploid genome of HAP1 cells ensures that IL11 disruption yields a uniform loss-of-function phenotype, as there is no second allele to compensate. This clean genetic background is advantageous for dissecting IL-11 signaling crosstalk with pathways such as TGF-?? and for performing unbiased genetic screens. HAP1??s robust growth and assay compatibility allow direct correlation of IL-11 loss with changes in proliferation, migration, and extracellular matrix production.
This knockout model is applicable to fibrosis research (cardiac, pulmonary, hepatic, renal), cancer studies (colorectal, gastric), inflammation, and drug target validation. Compatible techniques include western blotting, RT-qPCR, flow cytometry, phospho-STAT3 ELISA, collagen deposition, and proliferation/migration assays. For more information, contact Ascent Research.
