The ARID1B Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HeLa cervical carcinoma line. This product provides a loss-of-function model for the ARID1B gene, enabling investigation of its role in SWI/SNF-dependent chromatin remodeling and transcriptional regulation. The polyclonal format contains a heterogeneous pool of edited alleles, reflecting the diversity of CRISPR-mediated gene disruptions and offering robust population-level insights without clonal selection artifacts.
HeLa cells are a widely used human cervical adenocarcinoma line, originally isolated from an HPV18-positive tumor and characterized by epithelial morphology. This host cell model provides a well-established genetic and epigenetic background for studying oncogenic signaling, viral-host chromatin interactions, and the functional consequences of chromatin remodeler mutations in cancer.
ARID1B encodes a DNA-binding subunit of the BAF (SWI/SNF) ATP-dependent chromatin remodeling complex, where it directly interacts with core components ARID1A, SMARCA4, SMARCC1, and PBRM1. Its activity is regulated by upstream retinoic acid signaling and glucocorticoid receptor activation, and is targeted by microRNA miR-155. ARID1B controls the expression of downstream targets such as AXIN2, MYC, CCND1, and NEUROD1, thereby integrating signals from the Wnt/??-catenin and glucocorticoid receptor pathways to govern cell proliferation, differentiation, and DNA damage responses.
In the HeLa context, ARID1B knockout disrupts SWI/SNF-mediated chromatin remodeling, likely altering Wnt and cell cycle gene programs. This perturbation is particularly informative given HeLa cells?? expression of HPV18 E6/E7 oncoproteins, which independently disrupt tumor suppressors; the combined effect may model early stages of ARID1B-deficient cervical carcinogenesis. Additionally, the knockout simulates ARID1B loss-of-function seen in Coffin-Siris syndrome, offering a cell-based platform for studying neurodevelopmental gene regulatory defects.
These polyclonal knockout cells facilitate transcriptome analysis via RNA-seq, genome-wide profiling of histone modifications by ChIP-seq, and protein validation through western blotting. Functional assays including proliferation measurements, drug sensitivity testing, and immunofluorescence for chromatin marks are directly applicable. The model is suited for screening therapeutic compounds targeting ARID1B-deficient tumors and for dissecting SWI/SNF roles in DNA repair and epigenetic maintenance. For additional technical information, please contact Ascent Research.
