ALDH2 Knockout Jurkat Polyclonal Cells comprise a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T lymphocyte line, featuring targeted disruption of the ALDH2 gene. This cell product serves as a loss-of-function model to interrogate the mitochondrial aldehyde dehydrogenase ALDH2 and its central role in detoxifying acetaldehyde and other reactive aldehydes derived from endogenous and exogenous sources. The polyclonal format ensures representation of diverse editing events across the population, providing a robust tool for functional genomics studies without the need for single-cell cloning.
The parental Jurkat cell line is an immortalized T lymphocyte model originally isolated from the peripheral blood of a 14-year-old male diagnosed with acute T cell leukemia. Jurkat cells are a cornerstone in immunological research, extensively employed to dissect T cell receptor signaling, activation cascades, and leukemogenesis. Their active oxidative metabolism, particularly upon stimulation, renders them susceptible to redox imbalance and aldehyde toxicity, making them an ideal host for investigating ALDH2 function.
ALDH2 encodes a mitochondrial homotetrameric enzyme critical for the oxidation of acetaldehyde to acetate during ethanol metabolism, and also for the clearance of lipid peroxidation-derived aldehydes such as 4-hydroxy-2-nonenal (4-HNE). Its activity is tightly controlled by oxidative stress-sensitive transcription factors, notably Nrf2 (NFE2L2) and PPAR??, which upregulate ALDH2 expression in response to reactive oxygen species. ALDH2 acts in concert with other ethanol-metabolizing enzymes including alcohol dehydrogenase 1B (ADH1B), cytochrome P450 2E1 (CYP2E1), and catalase. Disruption of ALDH2 eliminates this detoxification axis, causing accumulation of genotoxic aldehydes that promote DNA damage, lipid peroxidation, and apoptosis, as summarized in the mechanistic profile of this knockout.
In Jurkat T lymphocytes, which undergo metabolic reprogramming and heightened oxidative phosphorylation during activation, ALDH2 deficiency leads to elevated intracellular levels of acetaldehyde and reactive aldehydes. This results in increased oxidative stress, as evidenced by enhanced ROS production, and triggers DNA damage responses, including phosphorylation of histone H2AX (??H2AX). Consequently, the knockout cells exhibit heightened sensitivity to ethanol and other aldehyde-generating insults, recapitulating key features of alcohol-induced cytotoxicity relevant to T cell biology and leukemia.
This polyclonal ALDH2 knockout product is tailored for a broad spectrum of downstream assays, including western blotting for ALDH2 protein, ALDH2 enzymatic activity measurement, acetaldehyde quantification, ROS detection using DCFDA, DNA damage analysis by ??H2AX immunostaining, apoptosis assessment via Annexin V, and cell viability assays under ethanol challenge. Researchers can apply this model to investigate T cell susceptibility to alcohol-induced toxicity, aldehyde-driven mutagenesis and carcinogenesis, oxidative stress responses in leukemia, and to screen for ALDH2 activators or inhibitors. For further information, please contact Ascent Research.
