ALDH16A1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the ALDH16A1 gene has been disrupted. This product provides a ready-to-use pooled population of HAP1 cells harboring heterogeneous knockout alleles, enabling functional genomics studies without the need for single-cell cloning. The knockout model serves as a versatile tool for investigating the role of ALDH16A1 in aldehyde metabolism and oxidative stress responses.
The HAP1 cell line is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells. It retains a single copy of most chromosomes, with the exception of disomy 8, and is widely used in genetic research due to its simplified karyotype. The haploid nature facilitates straightforward gene knockout and phenotypic analysis, making HAP1 an ideal host for CRISPR-based genome editing. Its leukemia origin also offers a relevant context for studying pathways involved in hematological malignancies and redox balance.
ALDH16A1 encodes an aldehyde dehydrogenase that catalyzes the NAD+-dependent oxidation of aldehydes, such as 4-hydroxynonenal (4-HNE) and malondialdehyde, to less reactive carboxylic acids. This enzymatic activity is critical for detoxifying products of lipid peroxidation. Under oxidative stress, ALDH16A1 expression is regulated by transcription factors including NRF2 (NFE2L2) and PPAR??. Functionally, ALDH16A1 interacts with the NAD+ cofactor and potentially with glutathione S-transferases to reduce 4-HNE protein adducts, thereby decreasing oxidative stress-induced NF-??B signaling. Disruption of ALDH16A1 therefore impairs the cellular capacity to mitigate aldehyde-induced damage, leading to accumulation of reactive aldehydes and heightened redox-sensitive signaling.
In HAP1 cells, ALDH16A1 knockout increases sensitivity to oxidative stress, as these leukemia-derived cells exhibit altered redox homeostasis. The near-haploid genotype ensures the knockout phenotype is unmasked, providing a clear loss-of-function effect. This polyclonal population enables robust study of aldehyde detoxification pathways and their impact on cell survival and stress responses in a hematological context. The model can also be used to assess how ALDH16A1 deficiency affects drug sensitivity, given the role of aldehydes in chemotherapeutic toxicity.
Typical applications include functional studies of ALDH16A1 in aldehyde metabolism, oxidative stress research, and drug toxicity testing. The model is suitable for ALDH activity assays, 4-HNE ELISA, cell viability assays under oxidative stress, and ROS flow cytometry. It also enables genetic screens for detoxification pathways and modeling of gout and hyperuricemia. For further information, please contact Ascent Research.
