CRISPR/Cas9-mediated gene disruption was employed to generate the CD36 Knockout HAP1 Polyclonal Cells, a heterogeneous population of HAP1 cells lacking functional CD36 protein. This polyclonal knockout product serves as a loss-of-function model for investigating the multi-ligand scavenger receptor CD36, facilitating studies of lipid metabolism, innate immunity, and inflammatory signaling. The knockout cell pool is suitable for applications requiring population-level phenotypic analysis without clonal selection.
The HAP1 cell line is a near-haploid human chronic myeloid leukemia cell line originally derived from the KBM-7 line. Its near-haploid karyotype simplifies genetic manipulation and eliminates the masking effects of a second allele, allowing for straightforward interpretation of knockout phenotypes. This adherent cell line retains key hematopoietic features while providing a robust and reproducible experimental system for functional genomics.
CD36 functions as a multi-ligand scavenger receptor that facilitates cellular uptake of oxidized low-density lipoprotein (oxLDL) and long-chain fatty acids. Its expression is transcriptionally upregulated by PPAR??, liver X receptor (LXR), and fatty acids, and downregulated by NRF2. Upon ligand engagement, CD36 associates with thrombospondin-1, integrins, and the Src-family kinases Fyn and Lyn, and cooperates with TLR2/TLR6 to activate downstream MAPK and NF-??B signaling cascades. This pathway promotes lipid accumulation and the secretion of pro-inflammatory cytokines, including TNF?? and IL-6, linking metabolic overload to inflammatory responses.
In the HAP1 background, disruption of CD36 provides a clean model to dissect CD36-dependent fatty acid transport and inflammatory signaling without interference from a functional second allele. The near-haploid state enhances the likelihood of complete loss-of-function and reduces genetic compensation, making this polyclonal population particularly valuable for high-throughput screening and quantitative biochemical assays. The model allows direct interrogation of how metabolic and immune signals converge through CD36 in a simplified leukemia-derived cellular environment.
Researchers can employ these CD36 Knockout HAP1 Polyclonal Cells in a wide range of experimental settings, including fatty acid uptake and oxLDL binding assays, lipid droplet staining with Oil Red O, flow cytometric analysis of surface receptor expression, RT-qPCR and western blotting for pathway components, ELISA-based measurement of cytokine secretion, and NF-??B luciferase reporter assays. The model is ideally suited for investigating mechanisms of atherosclerosis, diabetic cardiomyopathy, and metabolic syndrome, as well as drug screening for modulators of CD36-mediated lipid handling and inflammation. For additional technical information or to discuss customized gene editing services, please contact Ascent Research.
