The BCL11A Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional genomics studies. This product contains a heterogeneous pool of HEK293T cells carrying CRISPR-mediated disruptions at the BCL11A locus, offering a convenient loss-of-function model without the need for single-cell cloning.
The parental HEK293T cell line is a human embryonic kidney epithelial line established by transformation with adenovirus 5 DNA and stable expression of the SV40 large T antigen. These features enable high-efficiency transfection, robust protein expression, and efficient viral vector production, making HEK293T a workhorse for both basic and applied research.
BCL11A encodes a zinc finger transcriptional repressor that orchestrates hemoglobin switching by silencing fetal ??-globin (HBG1, HBG2) through recruitment of the NuRD corepressor complex (containing HDAC1, MTA1, MBD3). This activity is controlled by upstream regulators such as KLF1, GATA1, and SOX6. In B-lymphocytes, BCL11A regulates genes like BCL6, MYC, and ID2, and it is essential for early development. Additional roles in neurogenesis involve targets such as NEUROD1, and BCL11A intersects with Wnt signaling.
Although HEK293T cells are non-hematopoietic and do not express globins endogenously, the BCL11A knockout in this background allows researchers to study BCL11A’s transcriptional repression mechanisms and protein interactions in a tractable cellular context. The cells can be transfected with reporter constructs or cDNAs of erythroid/B-cell factors to reconstitute relevant complexes, or used directly to investigate BCL11A??s role in neuroepithelial and Wnt-related pathways.
Key applications include CRISPR-based functional genomics screens, mechanistic dissection of the BCL11A?CNuRD interaction by co-immunoprecipitation and ChIP, and screening for compounds that derepress ??-globin using reporter assays. The polyclonal knockout population is also suitable for RNA-seq, RT-qPCR, and Western blot analysis of target gene changes. For more information, contact Ascent Research.
