The ALDH1B1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HAP1 cells, with targeted disruption of the ALDH1B1 gene. This heterogeneous knockout model provides a loss-of-function system ideal for investigating aldehyde metabolism, retinoic acid signaling, and oxidative stress biology. As a polyclonal pool, it mitigates off-target and clonal variation effects, offering robust utility for functional genomic screens and pharmacological studies.
HAP1 cells are a near-haploid human cell line originating from KBM-7 chronic myeloid leukemia cells of a male patient. They exhibit an adherent, fibroblast-like morphology and a near-haploid karyotype, enabling single-copy gene disruptions to directly manifest as functional knockouts. This trait makes HAP1 cells particularly powerful for genetic screens, CRISPR-based functional genomics, and disease modeling.
ALDH1B1 is a mitochondrial NAD+-dependent aldehyde dehydrogenase that oxidizes aldehydes such as acetaldehyde and retinaldehyde into carboxylic acids. Its expression is regulated by transcription factors NRF2, PPAR??, and HNF4?? and is induced by ethanol and oxidative stress. Functionally, ALDH1B1 generates NADH and retinoic acid; the latter activates nuclear receptors RAR and RXR, thereby driving transcriptional programs. The enzyme interacts with cofactors NAD+ and CoA and works in concert with ALDH2, CYP2E1, and ADH to detoxify reactive aldehydes and preserve retinoic acid homeostasis, protecting cells from ethanol-induced damage.
In HAP1 cells, ALDH1B1 knockout disrupts aldehyde detoxification and retinoic acid biosynthesis, potentially sensitizing cells to ethanol toxicity and altering retinoic acid-dependent signaling. The near-haploid background simplifies interpretation of gene function by eliminating allelic compensation, making this model valuable for studying cancer metabolism, alcohol-related disease, and neurodegeneration associated with aldehyde accumulation.
This knockout model supports diverse applications: western blotting for ALDH1B1, ALDH enzyme activity assays, acetaldehyde toxicity challenges, NADH fluorescence measurements, RNA-seq pathway analysis, and MTT viability assays under ethanol stress. These enable investigations into alcohol-related liver disease, colorectal and pancreatic cancers, neurodegenerative disorders, and ALDH inhibitor screening. For additional information, please contact Ascent Research.
