The BACH1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the BACH1 gene in the human Jurkat T lymphocyte line. This pooled knockout model enables loss-of-function studies of the transcriptional repressor BACH1 without clonal selection, preserving cellular heterogeneity for broad phenotypic screening. CRISPR/Cas9-mediated gene disruption abrogates BACH1 protein expression, relieving repression of antioxidant response element (ARE)-regulated genes and facilitating investigation of BACH1-dependent regulatory networks in a T cell context.
The Jurkat cell line is an immortalized CD4+ T lymphocyte line originally derived from peripheral blood of a patient with acute T cell leukemia. These cells are extensively used as a model system for studying T cell receptor signaling, apoptosis, and HIV infection due to their well-characterized signaling pathways and ease of manipulation. Jurkat cells retain key features of T cell activation and gene expression, providing a relevant platform for examining redox-sensitive pathways and immune cell biology. The integration of BACH1 knockout into this host background allows dissection of BACH1??s role in T cell function, oxidative stress responses, and apoptotic signaling.
Mechanistically, BACH1 functions as a transcriptional repressor that heterodimerizes with small Maf proteins (MAFK and MAFG) and binds to ARE sites in the promoters of cytoprotective genes such as HMOX1 and NQO1. Under basal conditions, BACH1 suppresses these genes, while oxidative stress triggers NRF2 stabilization and FBXO22-mediated BACH1 degradation, leading to derepression of ARE-driven transcription. BACH1 additionally interacts with histone deacetylases to maintain chromatin in a repressed state. Beyond antioxidant defense, BACH1 regulates genes involved in cell cycle progression (cyclin D1), metastasis (CXCR4, MMP9), and ferroptosis, positioning it as a node linking redox balance, cancer biology, and immune cell function.
In Jurkat T cells, BACH1 knockout is anticipated to enhance basal and inducible expression of HMOX1 and NQO1, shifting the cellular redox poise toward increased antioxidant capacity. This alteration may modulate T cell activation thresholds, cytokine production, and susceptibility to activation-induced cell death, given the known roles of reactive oxygen species in T cell receptor signaling. Consequently, the BACH1 knockout Jurkat model provides a tool to interrogate the intersection of oxidative stress, immune signaling, and metabolic reprogramming in leukemia-derived lymphocytes, with implications for understanding T cell?Cdriven inflammation and immune surveillance.
This polyclonal knockout population supports a variety of research applications, including assessments of oxidative stress tolerance using ROS detection and cell viability assays, evaluation of ferroptosis sensitivity, and mechanistic studies of BACH1-dependent gene regulation via RT-qPCR for HMOX1 and NQO1, western blotting for BACH1 and NRF2, and ChIP-qPCR for ARE occupancy. It is also suited for migration and invasion assays to study metastasis-related pathways, and flow cytometric analysis of apoptosis to explore drug resistance mechanisms in a T cell background. For further technical details or custom inquiries, please contact Ascent Research.
