The ARID1B Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the ARID1B gene in HT29 cells. This heterogeneous pool provides a reliable loss-of-function model for studying ARID1B-dependent processes in a colorectal adenocarcinoma background. As a polyclonal population, it avoids clonal selection biases and is suitable for bulk assays requiring consistent knockout across a cell population. The product serves as an accessible tool for investigating SWI/SNF complex biology in an epithelial context.
HT29 is a human colorectal adenocarcinoma cell line with epithelial morphology, widely used as an intestinal epithelial model. It retains active Wnt/??-catenin and Notch signaling, key pathways in colorectal cancer. The cells are adherent, karyotypically stable, and amenable to genetic manipulation, making them a robust platform for CRISPR-based knockout studies. Their genetic background facilitates reproducible interrogation of chromatin remodeling events in malignancy.
ARID1B is a core DNA-binding subunit of the SWI/SNF chromatin remodeling complex, interacting with SMARCA4, SMARCA2, ARID1A, SMARCB1, SMARCC1, and SMARCD1. It regulates gene expression by altering nucleosome positioning at promoter regions. Upstream, transcription factors such as SP1 control ARID1B expression, while downstream targets include MYC, CCND1, CDKN1A, and ID genes. ARID1B integrates Wnt signaling through ??-catenin and Notch signaling via NOTCH1 and HES1, linking chromatin remodeling to proliferation and differentiation.
In colorectal cancer, ARID1B loss disrupts transcriptional programs that normally restrain proliferation, leading to dysregulated MYC and CCND1 expression. This model recapitulates SWI/SNF dysfunction seen in tumors, enabling analysis of how chromatin remodeling defects drive oncogenic phenotypes. Additionally, since ARID1B mutations cause neurodevelopmental disorders like Coffin-Siris syndrome, the HT29 knockout system offers a cell-based platform for exploring chromatin-related disease mechanisms. The epithelial context provides insight into how ARID1B coordinates cell fate decisions via the SWI/SNF complex.
Applications include Western blotting for ARID1B protein verification, RT-qPCR for target gene quantification, and ChIP-qPCR to measure SWI/SNF occupancy. Proliferation and apoptosis assays assess functional outcomes, while RNA-seq reveals transcriptome-wide changes. This polyclonal knockout population is a versatile resource for chromatin biology, cancer research, and neurodevelopmental disease modeling. For further inquiries, contact Ascent Research.
