The ALDH3A2 Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the ALDH3A2 gene in HAP1 cells. This product provides a heterogeneous pool of cells with targeted ALDH3A2 gene disruption, serving as a loss-of-function model for functional studies.
HAP1 is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells, exhibiting male origin, adherent growth, and fibroblast-like morphology. Its haploid nature simplifies gene editing and phenotypic analysis, making it a preferred system for genetic screening and functional genomics.
ALDH3A2 encodes a NAD+-dependent aldehyde dehydrogenase that oxidizes long-chain aliphatic aldehydes to fatty acids, critical for fatty aldehyde detoxification and sphingolipid metabolism. The enzyme operates as a homodimer and is transcriptionally activated by PPAR?? and NRF2, key regulators of lipid and oxidative stress responses. Its catalytic activity drives downstream pathways including fatty acid accumulation and mitigation of aldehyde-induced cytotoxicity. Knockout of ALDH3A2 disrupts these processes, leading to accumulation of cytotoxic fatty aldehydes and aberrant sphingolipid profiles.
In HAP1 cells, ALDH3A2 disruption recapitulates molecular hallmarks of Sj?gren-Larsson syndrome, an autosomal recessive disorder featuring ichthyosis and spastic paraplegia. The accumulation of fatty aldehydes induces oxidative stress and impairs cellular proliferation under aldehyde challenge, providing a physiologically relevant model. The haploid background enhances genotype-phenotype correlation, facilitating studies on peroxisomal lipid metabolism and the interplay between PPAR??/NRF2 signaling and sphingolipid homeostasis.
Research applications encompass fatty aldehyde detoxification, Sj?gren-Larsson syndrome modeling, and lipid metabolism investigations. Typical assays include aldehyde dehydrogenase activity measurements with hexadecanal substrate, fatty aldehyde quantification via LC-MS, ROS detection, and sphingolipid profiling. Proliferation assays under aldehyde stress and immunofluorescence further characterize the knockout phenotype. This polyclonal population is suitable for high-content screening and mechanistic dissection. For inquiries, contact Ascent Research.
