The CCL18 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HAP1 cells with targeted disruption of the CCL18 gene. This loss-of-function model is supplied as a pool of live knockout cells, avoiding the selection of a single clone. The polyclonal format provides genetic diversity while maintaining uniform ablation of CCL18 protein, making it suitable for chemokine signaling studies in a near-haploid human background.
The HAP1 cell line is a near-haploid human male line derived from the KBM-7 chronic myeloid leukemia model. Its stable haploid genome simplifies knockout generation and enables clean genetic interaction screens. As a hematological malignancy model, HAP1 retains cytokine and chemokine response pathways, offering a relevant context for examining genes involved in immune cell recruitment and tumor microenvironment dynamics. The cells exhibit rapid proliferation and adaptability to high-throughput assay formats.
CCL18 is a CC chemokine that acts as a chemoattractant for T cells, B cells, and dendritic cells. Its expression is upregulated by IL-4, IL-13, and STAT6, and it signals through the receptors CCR8 and PITPNM3, with subsequent activation of ERK1/2 and Akt. These downstream effectors regulate leukocyte migration and polarization. CCL18 also interacts with extracellular matrix glycosaminoglycans and is implicated in immune tolerance and tumor progression, linking to pathways such as JAK-STAT, MAPK, and PI3K-Akt.
In HAP1 cells, CCL18 knockout disrupts the CCR8/PITPNM3?CERK/Akt axis, attenuating migratory and polarization signals. The near-haploid background minimizes functional compensation from a second allele, yielding a robust loss-of-function model for studying chemokine-dependent crosstalk between leukemia cells and the microenvironment. This system closely replicates conditions relevant to tumor immune escape and can be used to test inhibitors targeting CCL18-driven pathways.
Typical applications include Transwell migration assays to measure chemotactic capacity, western blotting or phospho-ERK/Akt analysis to assess signal transduction, and flow cytometry for receptor profiling. ELISA confirms loss of chemokine secretion, and CRISPR-based functional screens exploit the polyclonal composition for genetic interaction studies. These cells are valuable for research in immunotherapy, tumor microenvironment modulation, chemokine signaling, and hematological malignancies, including asthma, arthritis, and solid tumors such as breast and hepatocellular carcinoma. Researchers may contact Ascent Research for further information.
