BCL7B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte line, designed for loss-of-function studies of the BCL7B gene. This product provides a heterogeneous pool of cells with targeted disruption of BCL7B, enabling robust investigation of its functional roles in chromatin remodeling and Wnt signaling without the need for single-cell cloning.
The Jurkat parental cell line originates from a patient with acute T cell leukemia and serves as a widely employed model for T-cell signaling, leukemia biology, and the molecular pathology of T-cell acute lymphoblastic leukemia (T-ALL). Jurkat cells exhibit constitutive activation of growth-promoting pathways including Wnt/??-catenin signaling, making them particularly relevant for dissecting the oncogenic mechanisms driven by aberrant transcription and chromatin dysregulation.
BCL7B is an integral subunit of the mammalian SWI/SNF (BAF) ATP-dependent chromatin remodeling complex and functions as a transcriptional coactivator in the Wnt/??-catenin pathway. Upon Wnt stimulation, ligands such as WNT3A engage FZD and LRP6 receptors, leading to inhibition of the destruction complex (AXIN, GSK3B) and stabilization of ??-catenin (CTNNB1). Nuclear ??-catenin associates with TCF/LEF transcription factors, notably TCF7L2, and recruits SWI/SNF complexes through direct interactions with BCL7B, SMARCA4, ARID1A, SMARCC1, and SMARCC2. This cooperative assembly remodels chromatin and drives transcription of critical target genes including MYC, CCND1, AXIN2, and LEF1. BCL7B knockout disrupts the coactivator bridge between ??-catenin and the remodeling machinery, impairing Wnt-dependent transcriptional output.
In the Jurkat T-ALL context, the Wnt/??-catenin cascade is often hyperactivated and contributes to leukemic proliferation through sustained expression of MYC and CCND1. BCL7B is positioned as a key mediator linking upstream signaling to chromatin-level gene activation. Disruption of BCL7B in these polyclonal knockout cells is therefore expected to attenuate target gene expression, resulting in reduced cell growth and enhanced apoptosis. This model enables researchers to examine the dependency of T-ALL cells on SWI/SNF-mediated coactivation and to explore therapeutic vulnerabilities associated with chromatin remodeling complexes.
These BCL7B knockout Jurkat polyclonal cells support a wide range of research applications, including functional dissection of the SWI/SNF complex in leukemia, mechanistic studies of Wnt-driven transcription, and validation of BCL7B as a potential therapeutic target. Representative assays include western blotting for BCL7B and downstream proteins, RT-qPCR for MYC and CCND1, RNA-seq for transcriptomic profiling, ChIP-qPCR for promoter occupancy, TCF/LEF luciferase reporter assays, and cell proliferation/apoptosis assays. The polyclonal format provides a rapid and cost-effective loss-of-function model for high-content functional genomics and preclinical drug discovery in hematologic malignancies and solid tumors. For further information, please contact Ascent Research.
