The ALDH7A1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human ALDH7A1 gene in the A-549 cell line. This product offers a genetically heterogeneous pool of cells with disrupted ALDH7A1 function, enabling loss-of-function studies without clonal selection. The polyclonal format preserves population diversity and is ideal for investigating aldehyde detoxification, lysine catabolism, and oxidative stress responses in a physiologically relevant alveolar epithelial model.
The host A-549 cell line is a widely used human lung adenocarcinoma model with adherent epithelial morphology, derived from alveolar basal epithelial cells. Retaining key characteristics of type II pneumocytes, such as surfactant production and responsiveness to oxidative stimuli, A-549 cells serve as a robust platform for pulmonary disease research and gene-editing applications, particularly in studying lung cancer and oxidative stress.
ALDH7A1 encodes a NAD+-dependent oxidoreductase that detoxifies aldehydes generated during lipid peroxidation and catalyzes the conversion of alpha-aminoadipic semialdehyde (AASA) to aminoadipate in the lysine degradation pathway. Its expression is transcriptionally regulated by NRF2 (NFE2L2) and PPARG in response to oxidative stress, linking it to the NRF2/KEAP1 antioxidant axis. The enzyme cooperates with aminoadipate-semialdehyde synthase (AASS) and utilizes NAD+ as a cofactor. Loss of ALDH7A1 leads to accumulation of L-1-piperideine-6-carboxylate (P6C), reduced NAD+ regeneration, and impaired clearance of lipid peroxidation products, thus compromising cellular defense against oxidative damage.
In the A-549 adenocarcinoma context, ALDH7A1 knockout sensitizes cells to oxidative damage and aldehyde toxicity, providing a relevant model for studying the interplay between detoxification capacity and cancer cell metabolism. This engineered system recapitulates features of oxidative stress-related disorders and pyridoxine-dependent epilepsy, enabling dissection of how impaired aldehyde clearance influences cancer phenotypes, lysine catabolism, and the NRF2/PPARG signaling network.
Researchers can employ these polyclonal knockout cells in a variety of assays, including western blotting and RT-qPCR for confirmation of gene disruption and downstream targets, ROS detection assays to quantify oxidative stress, aldehyde metabolite measurements to monitor pathway flux, and cell viability tests under oxidative challenge to assess chemosensitivity. The model is well-suited for exploring cancer metabolism, neurodegeneration mechanisms, and drug detoxification screening. For additional product information, please contact Ascent Research.
