The CCL22 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population designed to eliminate CCL22 expression in HAP1 cells. This loss-of-function model enables systematic investigation of CCL22-dependent signaling and cellular responses in a near-haploid background. By disrupting the gene encoding the chemokine (C-C motif) ligand 22, this product provides a genetically defined tool for dissecting chemokine-driven immune trafficking without the confounding influence of wild-type signaling.
The HAP1 host cell line is a human near-haploid cell model derived from the KBM-7 chronic myeloid leukemia line. These cells are male, hematopoietic in origin, and maintain a stable near-haploid karyotype, making them particularly suited for genetic screening applications. Their streamlined genome reduces genetic redundancy, facilitating unambiguous interpretation of knockout phenotypes. HAP1 cells have been widely adopted in functional genomics studies, including CRISPR-based screens and targeted gene disruption assays.
CCL22 is a chemokine ligand that activates the CCR4 receptor, a G??i-coupled GPCR. Its binding triggers downstream PI3K/AKT and MAPK/ERK pathways, promoting actin polymerization and directed cell migration. Expression is induced by IL-4 and IL-13 via STAT6, as well as by TNF-?? and CD40L through NF-??B. CCL22 serves as a chemoattractant for Th2 cells and regulatory T cells, and interacts with glycosaminoglycans to establish chemotactic gradients. Knockout of CCL22 disrupts CCR4-mediated signaling, inhibiting downstream effectors such as PI3K, AKT, and ERK, thus blocking chemotactic responses.
In HAP1 cells, the knockout provides a streamlined system to study chemokine signaling without diploid redundancy. The near-haploid karyotype ensures that disruption of a single allele yields a complete loss-of-function phenotype, enabling unambiguous genotype-phenotype correlations. This model eliminates CCR4-driven chemotaxis, making it ideal for screening CCR4 antagonists and investigating alternative chemokine pathways. It also permits interrogation of upstream regulatory networks involving IL-4/STAT6 and NF-??B in a simplified genomic context.
Applications include transwell migration assays to measure chemotaxis, calcium flux assays to monitor G??i signaling, and flow cytometry for receptor dynamics. RT-qPCR and western blotting validate target knockout and pathway changes. These cells are suitable for CCR4 antagonist development, tumor-immune evasion research, and allergic inflammation models such as asthma and atopic dermatitis. Researchers in immunology and cancer immunotherapy will benefit from this tool for dissecting Treg and Th2 recruitment. For product inquiries, contact Ascent Research.
