CCL8 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 cell line, targeting the CCL8 gene. The knockout product format is polyclonal, generated by CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous population with loss-of-function mutations in CCL8. This model enables functional studies of CCL8-dependent chemotactic signaling without the need for clonal isolation.
HAP1 cells are a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line, characterized by a fibroblast-like morphology and disomy of chromosome 8. They are BCR-ABL positive and widely used in functional genomics and CRISPR knockout screens due to their haploid karyotype, which simplifies gene editing and phenotypic characterization. The cells provide a robust platform for investigating gene function in a simplified genetic context.
CCL8, a CC chemokine, acts as a chemoattractant for monocytes, T cells, NK cells, and basophils. It is upregulated by proinflammatory stimuli such as IL-1??, TNF-??, IFN-??, and LPS, through transcription factors including NF-??B and STAT3. CCL8 binds to chemokine receptors CCR1, CCR2, and CCR5, initiating G protein-coupled signaling cascades. Downstream, it activates the PI3K/AKT and MAPK/ERK pathways, promoting cell migration and inflammatory cytokine production. Knockout of CCL8 disrupts these axes, impairing chemotactic responses and attenuating signal transduction through these pathways.
In HAP1 cells, loss of CCL8 provides a clean background to dissect chemokine receptor signaling independently of endogenous ligand interference. The near-haploid genome reduces functional redundancy, making phenotypic changes more directly attributable to CCL8 disruption. This model is particularly suited for studying the role of CCL8 in modulating JAK/STAT and NF-??B pathways, as well as for validating the specificity of CCR antagonists. It also facilitates investigation of crosstalk between integrin-mediated adhesion and chemokine-directed migration in a BCR-ABL positive leukemic environment.
This polyclonal knockout population is ideal for a range of applications including chemotaxis assays to measure cell migration, Western blotting and RT-qPCR for confirmation of CCL8 disruption, phospho-specific immunoblotting to assess AKT and ERK activation, and ELISA for secreted chemokine profiling. It can be used to study inflammatory disease mechanisms, cancer metastasis, and autoimmune disorders. The model supports drug target validation for CCR inhibitors and functional genomics screens. For further details, please contact Ascent Research.
