The BCL7C Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the BCL7C gene. This product provides a heterogeneous pool of edited cells generated by CRISPR/Cas9-mediated gene disruption, offering a versatile model for investigating BCL7C-dependent pathways without the need for clonal isolation.
The HAP1 host cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) blast crisis line, characterized by a male karyotype with a single copy of most chromosomes. This unique genetic background enables efficient haploid genetic screens, functional genomics, and gene-editing experiments, making HAP1 an ideal system for dissecting gene function in a leukemic context.
BCL7C functions as a tumor suppressor and an integral subunit of the SWI/SNF (BAF) chromatin remodeling complex. It directly interacts with core BAF components including SMARCA4, SMARCA2, ARID1A, and SMARCB1 to modulate chromatin accessibility and transcriptional regulation. BCL7C acts downstream of MYC-mediated transcriptional control and regulates key target genes such as CCND1, a cyclin involved in cell cycle progression, as well as pro-apoptotic factors. Disruption of BCL7C compromises BAF complex integrity, leading to altered expression profiles that promote uncontrolled proliferation and evade apoptosis, thereby contributing to oncogenesis.
In the HAP1 leukemic background, BCL7C knockout provides a relevant model to study the consequences of SWI/SNF complex dysfunction. As BCL7C loss is implicated in acute lymphoblastic leukemia, non-Hodgkin lymphoma, and solid tumors with SWI/SNF mutations, this knockout population enables the investigation of tumor suppressor mechanisms and the identification of synthetic lethal interactions specific to BAF complex perturbations within a near-haploid, leukemia-derived environment.
Researchers can utilize these polyclonal knockout cells in a broad array of assays, including chromatin immunoprecipitation sequencing (ChIP-seq) to map genome-wide changes in chromatin occupancy, co-immunoprecipitation to assess BAF complex assembly, quantitative RT-PCR to measure downstream gene expression, and functional studies such as Annexin V apoptosis assays or cell cycle analysis. Drug sensitivity assays can further reveal vulnerabilities induced by BCL7C loss. The BCL7C Knockout HAP1 Polyclonal Cells serve as a critical resource for advancing SWI/SNF biology and leukemia research. For further details, please contact Ascent Research.
