The EBPL Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HAP1 cell line, designed for loss-of-function studies of the EBPL gene. This product provides a mixed population of gene-edited cells, enabling researchers to investigate the functional consequences of EBPL disruption without single-cell cloning, reflecting the heterogeneity of knockout effects in a physiologically relevant model.
The HAP1 host cell line is a near-haploid, human chronic myeloid leukemia-derived cell line with an adherent, fibroblast-like morphology. Originating from KBM-7 cells, HAP1 retains wild-type p53 function. Its near-haploid karyotype simplifies genetic manipulation, as most genes exist in a single copy, facilitating studies of gene function without allelic variation. This model is particularly advantageous for metabolic studies where gene dosage effects are critical.
EBPL encodes a homolog of emopamil binding protein (EBP) and is predicted to function as a sterol isomerase in the cholesterol biosynthesis pathway, regulated by SREBP1, SREBP2, and LXR. EBPL acts downstream of HMGCR, SQLE, LSS, and FDFT1, and upstream of CYP51A1, EBP, DHCR7, and DHCR24, interacting with EBP, SC4MOL, and NSDHL. Disruption of EBPL may alter cholesterol synthesis, impacting Sonic Hedgehog signaling and membrane lipid composition, which are critical for cell growth and differentiation.
In the HAP1 cell model, loss of EBPL provides a tool for dissecting cholesterol metabolism in a leukemic context. Chronic myeloid leukemia cells often exhibit altered lipid metabolism, and the near-haploid background enables clean genotype-phenotype correlations. This knockout model helps examine how sterol isomerase activity affects cancer cell viability, response to statins, and lipid storage, contributing to understanding metabolic vulnerabilities in leukemia.
Typical applications include functional studies of cholesterol biosynthesis, screening for modulators of sterol metabolism, and off-target analysis of cholesterol-lowering drugs. Assays include RT-qPCR for gene expression, western blot for sterol regulatory proteins, cholesterol quantification, lipidomics profiling, filipin staining, and cell proliferation under lipid-depleted conditions. Drug sensitivity assays with statins can be employed to study cancer metabolism. For further details, please contact Ascent Research.
