The APOA2 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in the HAP1 human cell line, targeting the APOA2 gene. This loss-of-function model enables detailed investigation of apolipoprotein A-II function in high-density lipoprotein (HDL) biology and reverse cholesterol transport, providing a critical tool for lipid metabolism research.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line. These cells are BCR-ABL1 positive and originate from a male donor. The near-haploid karyotype simplifies knockout generation, as disruption of a single allele typically abolishes gene expression, making HAP1 a powerful host for functional genomics and haploid genetic screens in cancer research.
The APOA2 gene encodes apolipoprotein A-II (apoA-II), a major structural protein of HDL particles. ApoA-II stabilizes HDL architecture and modulates enzymes and lipid transfer proteins essential for reverse cholesterol transport. Its transcription is activated by nuclear receptors PPAR??, LXR, and FXR, and is influenced by insulin and glucose. ApoA-II interacts with APOA1, APOC3, APOE, CETP, PLTP, LCAT, and hepatic lipase, and regulates downstream processes including HDL particle size distribution, cholesterol efflux capacity, and CETP activity. Within the reverse cholesterol transport pathway, APOA2 functions alongside APOA1, LCAT, CETP, PLTP, SR-BI, ABCA1, and ABCG1.
In the HAP1 cellular context, APOA2 knockout leverages the near-haploid background to ensure functional nullity, enabling unambiguous dissection of apoA-II-dependent lipid handling. This model is particularly pertinent for exploring how apoA-II deficiency influences lipid trafficking within a leukemic context, potentially revealing crosstalk between BCR-ABL1 oncogenic signaling and HDL metabolism.
Applications include HDL metabolism studies, reverse cholesterol transport assays, lipid metabolism research, and drug screening for dyslipidemia. The polyclonal format is ideal for haploid genetic screens to uncover lipid transport regulators. Compatible assays encompass APOA2 western blotting, cholesterol efflux assays, RT-qPCR of lipid genes (e.g., ABCA1, SR-BI), HDL particle sizing, RNA-seq, and lipidomics. Additionally, these cells can be employed in co-culture systems to examine hepatocyte-like lipid transfer mechanisms. For further technical details, please contact Ascent Research.
