BRWD1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HeLa cervical adenocarcinoma cell line. This product comprises a heterogeneous pool of cells carrying CRISPR/Cas9-mediated gene disruption at the BRWD1 locus, leading to functional loss of the encoded chromatin remodeling scaffolding protein. It serves as a versatile loss-of-function model for studying BRWD1-dependent processes in an epithelial background.
HeLa cells are an immortalized epithelial line originating from a human cervical adenocarcinoma, widely employed as a model for cervical cancer and general epithelial cell biology. Their robust growth, extensive molecular characterization, and sensitivity to DNA damage make them a practical platform for investigating gene functions related to oncogenesis, repair pathways, and chromatin dynamics. Although not of lymphoid origin, HeLa cells express conserved chromatin remodeling and DNA repair components, allowing dissection of BRWD1??s core mechanistic roles.
BRWD1 operates as a scaffolding subunit of the SWI/SNF (BAF) chromatin remodeling complex, binding to core ATPase SMARCA4 (BRG1), SMARCC1, and ACTL6A, and recognizing acetylated histones H3 and H4. This targeting facilitates nucleosome repositioning and DNA accessibility at promoters and enhancers. In B cells, BRWD1 is indispensable for recruiting RAG1/RAG2, AID, and 53BP1 to immunoglobulin loci for V(D)J recombination and class switching, downstream of B cell receptor activation, CD40?CCD40L, and NF-??B signals. It transcriptionally regulates AICDA and UNG, key for antibody diversification. Knockout disrupts these complexes, impairing DNA break formation and repair at specific genomic sites.
In the HeLa context, BRWD1 knockout enables exploration of its broader chromatin regulatory functions relevant to cervical cancer. Loss of BRWD1 may alter SWI/SNF genome-wide localization, affecting expression of genes involved in proliferation, DNA repair, and epithelial-mesenchymal transition. This model can be used to uncover synthetic vulnerabilities, investigate drug sensitivities, or study chromatin-mediated control of HPV oncogene expression. Bridging immunology and cancer biology, the cells offer a platform to compare BRWD1??s role in DNA repair between lymphoid and epithelial systems.
Applications include ChIP-seq to profile BRWD1-dependent chromatin landscapes, RNA-seq for transcriptomic effects, and co-immunoprecipitation to map interaction changes. Functional assays such as proliferation, migration, and cell viability testing are readily performed. Compound screens can identify modulators of BRWD1-related pathways. For DNA recombination studies, these cells provide an epithelial counterpart to B-cell models, aiding mechanistic dissection. For further details, contact Ascent Research.
