The BEND4 Knockout HEK293T Polyclonal Cells are a ready-to-use human cell reagent consisting of a population of HEK293T cells that have been subjected to CRISPR/Cas9-mediated disruption of the BEND4 locus. As a polyclonal knockout pool, this product provides a genetically heterogeneous collection of cells, each carrying distinct loss-of-function mutations, enabling robust functional genomics studies without the bottleneck of single-cell cloning.
The HEK293T host cell line is a widely utilized derivative of the human embryonic kidney HEK293 line, distinguished by stable expression of the SV40 large T antigen. This antigene enhances episomal replication of transfected plasmids containing the SV40 origin, making HEK293T cells ideal for high-efficiency transient transfection, protein overexpression, retroviral and lentiviral production, and scalable recombinant protein manufacturing. The cells exhibit an adherent epithelial morphology and originate from female tissue.
BEND4 encodes a BEN domain-containing protein implicated in transcriptional repression through the recruitment of chromatin-modifying complexes, such as the NuRD complex, to specific genomic loci. This activity is associated with the deposition of repressive histone modifications, including H3K27me3, leading to silencing of target gene promoters. BEND4 function is regulated by upstream developmental and signaling cues, including effectors of the Wnt, TGF-beta, and Notch pathways. Its downstream targets encompass genes governing cell cycle progression, neuronal differentiation, and apoptosis, positioning BEND4 at a nexus of proliferation control and cell fate determination.
Within the HEK293T cellular context, disruption of BEND4 offers a powerful system to dissect its role in transcriptional regulation and chromatin biology. Given the kidney epithelial origin of the host, this knockout model is particularly relevant for exploring BEND4’s function in epithelial homeostasis and its potential tumor-suppressive activities, as BEND4 inactivation has been linked to colorectal and gastric cancers. Moreover, the high transfectability of HEK293T cells allows seamless introduction of additional genetic perturbations or reporters, facilitating complementation studies and pathway mapping.
This BEND4 knockout polyclonal cell population empowers a wide array of experimental approaches, including RT-qPCR and Western blotting for knockout verification, RNA-seq for global transcriptome profiling, and ChIP-seq to assess changes in histone modification landscapes. Functional assays such as proliferation, colony formation, and migration/invasion tests can be deployed to evaluate the impact on cell growth and motility, while drug sensitivity screens help identify compounds that selectively target BEND4-deficient cells. The versatility of the HEK293T background further supports lentiviral packaging and large-scale biochemical studies. For further information or to request a quote, please contact Ascent Research.
