The CCRL2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 chronic myeloid leukemia (CML) cell line. This product features targeted disruption of the CCRL2 gene via CRISPR/Cas9-mediated gene editing, resulting in a loss-of-function model for the atypical chemokine receptor CCRL2 in a diploid-like, near-haploid background. The polyclonal format provides a heterogeneous pool of edited cells suitable for bulk functional assays, eliminating the need for single-cell cloning while retaining the flexibility of a mixed population.
The HAP1 host cell line is a near-haploid, fibroblast-like cell line derived from the KBM-7 CML line. HAP1 cells maintain a near-haploid karyotype (excluding a disomy of chromosome 8), making them an ideal platform for haploid genetic screens, functional genomics, and gene-loss studies. Their male origin and chronic myeloid leukemia background provide a unique model for studying hematological malignancies and inflammation-related signaling networks in a genetically simplified, yet biologically relevant, system.
CCRL2 is an atypical chemokine receptor that functions as a decoy receptor, binding and internalizing the chemotactic ligands chemerin (RARRES2) and CCL19 without activating canonical G-protein signaling. This scavenging activity is mediated through clathrin-mediated endocytosis and ??-arrestin-2 recruitment. Upstream regulators such as TNF-??, IL-1??, NF-??B, and hypoxia modulate CCRL2 expression. Knockout of CCRL2 disrupts this scavenging, leading to elevated extracellular chemerin and CCL19 levels, which in turn potentiate CMKLR1 and CCR7 signaling pathways. Downstream consequences include enhanced leukocyte recruitment and upregulation of pro-inflammatory cytokines like IL-6 and CXCL8.
The utility of the CCRL2 Knockout HAP1 Polyclonal Cells lies in the convergence of a defined genetic knockout with the HAP1 line??s near-haploid genome. This combination allows robust, high-throughput functional studies of chemokine scavenging mechanisms without the confounding gene-dose effects typical of diploid models. In the context of chronic inflammation, cancer, or atherosclerosis research, this model enables direct assessment of CCRL2??s role in regulating chemokine gradients and immune cell migration. The polyclonal nature ensures representation of diverse editing events, reducing clonal bias in downstream assays while maintaining sufficient knockout efficiency for population-based analyses.
These cells can be used in chemokine scavenging assays, chemotaxis/migration assays, flow cytometry for ligand binding, ELISA, and co-immunoprecipitation to assess CCRL2 function. They are well-suited for haploid genetic screens to identify chemokine signaling modulators. This model supports drug target validation in inflammatory diseases and cancer. For further technical specifications or ordering information, please contact Ascent Research.
