ECH1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for the targeted disruption of the ECH1 gene encoding peroxisomal enoyl-CoA hydratase in the HAP1 near-haploid human cell line. This polyclonal knockout model provides a genetically heterogeneous pool of edited cells, facilitating robust functional interrogation of ECH1-dependent processes without subcloning artifacts.
HAP1 is a leukemia-derived, near-haploid human cell line (male origin) adapted for adherent growth, originally derived from KBM-7 chronic myeloid leukemia cells. With disomy only of chromosome 8 and a portion of chromosome 15, its near-haploid karyotype reduces genetic redundancy, making it exceptionally suitable for knockout and functional genomics screens.
ECH1 encodes a peroxisomal enzyme that catalyzes the second step of fatty acid beta-oxidation, hydrating trans-2-enoyl-CoA to 3-hydroxyacyl-CoA. As a core component of the peroxisomal beta-oxidation pathway, ECH1 functions downstream of ACOX1 and upstream of HSD17B4, interacting with peroxisomal biogenesis factors PEX5 and PEX14. Its activity is regulated by the PPARA/RXRA heterodimer, with transcriptional control exerted by PPARA, NFE2L2 (NRF2), and PGC1A. Disruption of ECH1 leads to accumulation of very long-chain fatty acids, perturbing PPAR??-mediated transcriptional responses and cellular lipid homeostasis.
In the HAP1 near-haploid context, ECH1 knockout creates a potent system for studying peroxisomal function and lipid metabolism. The absence of ECH1 impairs the degradation of very long-chain fatty acids, mimicking metabolic defects observed in peroxisomal disorders, metabolic syndrome, and non-alcoholic fatty liver disease. Furthermore, given the role of fatty acid oxidation in cancer metabolic reprogramming, this knockout model serves as a valuable tool for investigating how ECH1 loss influences tumor cell survival and energy metabolism. Its haploid nature facilitates clear genotype-phenotype correlations, enhancing the interpretability of observed metabolic shifts.
This product is ideally suited for a range of advanced applications, including peroxisomal biology studies, metabolic disease modeling, and cancer metabolism research. Researchers can employ assays such as Western blotting for ECH1 depletion verification, RT-qPCR for PPARA-target gene expression, VLCFA accumulation quantification, lipidomics mass spectrometry, Seahorse metabolic flux analysis, and immunofluorescence for peroxisome visualization. Additionally, co-immunoprecipitation can probe disrupted protein interactions, and cell viability assessments under lipid stress can reveal functional consequences of ECH1 loss. These polyclonal knockout cells also enable high-throughput functional genomics screens and drug discovery programs targeting fatty acid oxidation-related disorders. For additional details, please contact Ascent Research.
