The BACH1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited pooled knockout population, designed for functional loss-of-function studies of the BACH1 gene. This product comprises a heterogeneous pool of HAP1 cells carrying targeted disruptions of the BACH1 locus, generated via non-clonal gene editing. The polyclonal format minimizes clonal selection bias and provides a robust model for investigating BACH1-dependent signaling in a near-haploid human leukemic background.
HAP1 cells are a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia line, exhibiting adherent, fibroblast-like morphology. Their haploid karyotype simplifies genetic manipulation and facilitates haploid genetic screens, making HAP1 a versatile host for studying gene function in a leukemic context. This background is particularly suitable for dissecting pathways involved in oxidative stress and drug sensitivity, as leukemic cells often exhibit altered redox homeostasis.
BACH1 encodes a transcriptional repressor that competes with NRF2 for binding to antioxidant response elements (AREs). Under basal conditions, BACH1 heterodimerizes with small Maf proteins to repress genes like HMOX1 and NQO1. Oxidative stress or heme accumulation promotes heme binding to BACH1, causing its displacement, FBXO22-mediated degradation, and permitting NRF2-driven activation of cytoprotective transcription. Regulators such as KEAP1, HIF-1??, and PI3K/AKT influence BACH1 activity, while downstream targets include HMOX1, NQO1, CXCR4, and MMPs, linking BACH1 to ferroptosis, heme metabolism, and cancer cell migration.
In the HAP1 host cell model, disruption of BACH1 function serves as a valuable tool to interrogate the NRF2?Cantioxidant axis within a leukemic background. Given the importance of reactive oxygen species (ROS) management in leukemia cell survival and drug resistance, these polyclonal knockout cells enable the investigation of heme homeostasis, ferroptosis susceptibility, and chemoresistance mechanisms. The polyclonal nature of the knockout population allows researchers to assess phenotypic outcomes without the confounding effects of single-cell adaptation, providing a more physiologically relevant model system.
Researchers can employ BACH1 Knockout HAP1 Polyclonal Cells in a variety of assays, including western blotting to confirm BACH1 loss and HMOX1 induction, RT-qPCR for antioxidant gene profiling, ARE-luciferase reporter assays to measure NRF2 transcriptional activity, ROS detection using fluorescent probes, and ferroptosis sensitivity tests with inducers such as erastin or RSL3. These cells are also suitable for migration and invasion studies and heme quantification in metastasis models. Typical applications span cancer biology, drug resistance studies, and neurodegenerative disease research. For further technical details, please contact Ascent Research.
