In Stock Cell Lines
The Gstm2 Knockout AML12 Cell Line is a CRISPR/Cas9-edited loss-of-function model for glutathione S-transferase mu 2 in non-tumorigenic mouse hepatocytes. Gstm2 encodes a phase II enzyme that conjugates glutathione to electrophilic toxins, protecting cells from oxidative stress; its expression is regulated by NFE2L2 and KEAP1. AML12 cells retain core hepatocyte functions, enabling drug metabolism profiling and hepatotoxicity screening. Applications include GST activity assays, ROS detection, and pathway analysis of factors like NFE2L2. For details, contact Ascent Research.
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ARHGEF18 Knockout AGS Polyclonal Cells
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DES Knockout Raji Polyclonal Cells
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Rat Renal Epithelial Cell Medium
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The Gstm2 Knockout AML12 Cell Line provides a CRISPR/Cas9-edited loss-of-function model of glutathione S-transferase mu 2 (GSTM2) in mouse hepatocytes. This product disrupts the Gstm2 gene, eliminating GSTM2 enzyme activity to enable studies of phase II detoxification and oxidative stress responses without endogenous background. The knockout line offers a clean genetic system to assess cellular vulnerability to electrophilic compounds.
The AML12 cell line, derived from a transgenic mouse expressing human TGF-??, is non-tumorigenic and retains core hepatocyte functions such as metabolism, detoxification, and protein synthesis. This physiologically relevant model maintains cytochrome P450 activity and intact glutathione pathways, making it an ideal host for investigating hepatic drug metabolism and stress responses in a genetically defined background.
Gstm2 encodes a phase II enzyme that conjugates reduced glutathione (GSH) to electrophilic xenobiotics and endogenous reactive species, neutralizing toxicity and promoting excretion. Its transcription is controlled by the KEAP1-NFE2L2 (Nrf2) pathway: oxidative stress triggers NFE2L2 release from KEAP1, leading to antioxidant response element activation. The aryl hydrocarbon receptor (AHR) also regulates Gstm2. GSTM2 activity reduces intracellular reactive oxygen species (ROS) and modulates JNK1-mediated apoptosis. The enzyme operates within a network involving glutamate-cysteine ligase (GCL) for GSH synthesis, glutathione reductase (GSR) for GSH regeneration, and cytochrome P450 enzymes that generate substrates.
In AML12 hepatocytes, Gstm2 knockout removes a key defense against electrophilic and oxidative injury. These cells normally depend on GSTs for detoxification; Gstm2 loss heightens susceptibility to drug-induced toxicity and ROS. This model isolates the specific role of GSTM2 in hepatocyte stress resilience, enabling examination of compensatory mechanisms from other GST isoforms or antioxidants, and evaluation of JNK1 signaling and apoptosis thresholds.
Applications include drug metabolism profiling, hepatotoxicity screening, and oxidative stress studies. Users can quantify cell viability under electrophilic stress, measure ROS, and perform GST activity assays using CDNB. Western blotting and RT-qPCR confirm gene disruption and monitor NFE2L2, KEAP1, and GCL expression. This line also supports cancer susceptibility studies of impaired phase II detoxification. For support, contact Ascent Research.
