CCR3 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the CCR3 gene in the HAP1 human myeloid leukemia cell line. This loss-of-function model is produced by CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of cells with CCR3 knockout, ideal for functional studies in a near-haploid genetic background. The polyclonal format provides a robust system free from clonal variation, and the cells are supplied as a frozen stock ready for expansion.
The HAP1 cell line is a near-haploid human myeloid leukemia line derived from KBM-7 chronic myeloid leukemia cells. Its near-haploid karyotype simplifies genetic analysis by eliminating confounding effects of diploid alleles, making it a preferred model for genetic screens and receptor pharmacology. HAP1 cells exhibit rapid growth and are amenable to high-throughput transfection and assay protocols, and their adherent morphology and stable genomic characteristics further support reproducible experimentation.
CCR3 is a G protein-coupled receptor that binds eotaxin chemokines (CCL11, CCL24, CCL26) and transduces signals through G??i proteins. Upon activation, G??i mediates intracellular calcium release via PLC??-IP3 pathways and activates PI3K??-Akt-Rac signaling, leading to PAK-LIMK-cofilin-driven actin polymerization essential for eosinophil migration. The receptor also stimulates MAPK cascades, including ERK1/2 phosphorylation, promoting chemotaxis and degranulation. CCR3 expression is upregulated by IL-4 and IL-13, and receptor activity is modulated by ??-arrestins 1/2, GRK2/5, and RGS proteins, which regulate desensitization and signal duration. These signaling networks coordinate cytoskeletal reorganization and cellular adhesion responses central to allergic inflammation.
In the HAP1 near-haploid context, CCR3 knockout yields a clear loss-of-function phenotype without interference from a wild-type allele, facilitating unambiguous interpretation of signaling pathway contributions. The polyclonal knockout population captures population-level responses and avoids clonal artifacts, enabling reproducible investigation of CCR3-dependent processes such as calcium mobilization and chemotaxis. This model is particularly relevant for studying eosinophil biology given the myeloid lineage of HAP1 cells.
These cells support diverse research applications, including target validation for eosinophil-associated disorders like asthma, allergic rhinitis, and eosinophilic esophagitis, as well as high-throughput screening for novel pharmacological modulators. Compatible assays include Boyden chamber chemotaxis, calcium flux measurements, flow cytometry for surface protein detection, western blotting for phospho-ERK1/2 and phospho-Akt, and immunofluorescence for actin dynamics. For further information or to discuss specific experimental needs, please contact Ascent Research.
