The BCL7B Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 human haploid fibroblast-like cell line. This product provides a heterogeneous pool of cells harboring disruptions in the BCL7B gene locus, enabling loss-of-function studies without clonal artifacts.
HAP1 is a near-haploid human cell line originally derived from a male chronic myeloid leukemia patient in blast crisis. With a predominantly haploid karyotype (except for disomy of chromosome 8), HAP1 cells are exclusively amenable to genetic manipulation and are widely employed in haploid genetic screens and targeted knockout experiments. Their adherent, fibroblast-like morphology and stable growth characteristics make them a robust platform for functional genomics research.
BCL7B encodes a subunit of the SWI/SNF chromatin remodeling complex, interacting with core ATPases SMARCA4 (BRG1) and SMARCA2 (BRM), along with scaffold proteins ARID1A, SMARCC1, and SMARCC2, to regulate transcription. It also associates with BCL7A and BCL7C. Through the SWI/SNF complex, BCL7B antagonizes Wnt signaling downstream of the Frizzled receptor and Dishevelled, counteracting ??-catenin/TCF-LEF-mediated activation. The upstream regulators Wnt3a and ??-catenin modulate BCL7B activity, while p53 and MYC also influence its expression. Downstream, BCL7B loss alters transcription of MYC, CCND1 (Cyclin D1), BCL2, BAX, and CDKN1A (p21), linking chromatin remodeling to cell cycle, apoptosis, and proliferation.
Disruption of BCL7B in the HAP1 background abrogates its incorporation into the SWI/SNF complex, impairing chromatin remodeling and altering the transcriptional output of Wnt target genes. This loss-of-function model recapitulates aspects of tumor suppressor inactivation observed in lymphomas, lung adenocarcinomas, and B-cell malignancies. The haploid nature of HAP1 ensures that single-gene disruptions yield clear phenotypic outcomes, making this polyclonal knockout pool a powerful tool for dissecting BCL7B??s role in SWI/SNF-driven transcriptional programs and Wnt pathway dysregulation.
Researchers can employ these BCL7B knockout HAP1 polyclonal cells in a variety of functional assays, including chromatin immunoprecipitation (ChIP-qPCR) to assess SWI/SNF occupancy at target promoters, transcriptomic profiling via RNA-seq to identify dysregulated Wnt-responsive genes, and flow cytometry to evaluate cell cycle perturbations and apoptosis. Additionally, the cells are suitable for colony formation assays, xenograft tumor growth studies, and drug sensitivity screening with Wnt inhibitors, facilitating both mechanistic studies and translational applications in cancer biology. For further details, please contact Ascent Research.
