The BCL7C Knockout Jurkat Polyclonal Cells are a heterogeneous population of CRISPR/Cas9-edited Jurkat T lymphoblastoid cells carrying a targeted disruption in the BCL7C tumor suppressor gene. This polyclonal knockout pool provides a versatile loss-of-function model for investigating SWI/SNF chromatin remodeling complex activity in a T lymphocyte context. The absence of functional BCL7C protein enables robust interrogation of downstream transcriptional and phenotypic consequences without selection for clonal genotypes. These cells are intended for research applications in molecular oncology, immunology, and epigenetics.
The parental Jurkat cell line is an immortalized T lymphoblastoid model derived from an acute T cell leukemia patient and transformed with human T-lymphotropic virus type I (HTLV-I). Jurkat cells are used for studying T cell receptor signaling, apoptosis, and HIV infection, owing to their well-characterized signal transduction pathways and rapid proliferation. This established cell background provides a reproducible system for evaluating gene function within a leukemic T cell environment, making it particularly suitable for dissecting tumor suppressor mechanisms in lymphoid malignancies.
BCL7C functions as a core subunit of the SWI/SNF ATP-dependent chromatin remodeling complex, which orchestrates nucleosome positioning to regulate gene expression. As a tumor suppressor, BCL7C participates in complexes containing SMARCA4, SMARCB1, ARID1A, and ACTL6A, and its loss is associated with aberrant transcriptional programs in lymphomas. Mechanistically, BCL7C knockout impairs SWI/SNF-mediated chromatin accessibility, altering the expression of cell cycle regulators and apoptotic genes. Upstream regulators such as chromatin modifiers and transcription factors modulate BCL7C activity, while the complex directly targets genes involved in cell cycle progression and programmed cell death.
In the Jurkat T-cell environment, BCL7C disruption provides a powerful platform to dissect SWI/SNF-dependent gene regulatory networks that govern T lymphocyte growth and survival. Although BCL7C mutations are primarily linked to diffuse large B-cell and other B-cell lymphomas, the fundamental chromatin remodeling function is conserved across lineages. This model allows researchers to examine how loss of a key SWI/SNF subunit influences transcriptional landscapes, cell cycle dynamics, and apoptotic thresholds in a T-cell leukemia setting. It offers insight into the tumor-suppressive role of chromatin remodeling complexes beyond their classical disease associations.
Researchers can employ these polyclonal knockout cells in advanced applications, including RNA-seq to map transcriptional changes, ChIP-qPCR to quantify SWI/SNF occupancy, and co-immunoprecipitation to assess complex integrity with partners like SMARCA4 and ARID1A. Flow cytometry for annexin V binding or cell cycle distribution enables phenotypic characterization. Western blotting and RT-qPCR confirm BCL7C depletion, supporting mechanistic studies in lymphomagenesis. For further information, please contact Ascent Research.
