The ARID1B Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional genomics and chromatin remodeling research. This product consists of a heterogeneous pool of HAP1 cells harboring targeted gene disruptions in ARID1B, offering a robust loss-of-function model to study ARID1B-dependent cellular processes. The polyclonal format avoids clonal artifacts, providing a representative population-level readout suitable for high-content screening and pooled functional assays.
The HAP1 host cell line is a near-haploid human chronic myeloid leukemia (CML) derivative of the KBM-7 cell line, characterized by adherent growth and p53 deficiency. Its near-haploid genome simplifies gene targeting and facilitates efficient knockout generation by minimizing the need for biallelic inactivation. HAP1 cells exhibit a hematopoietic progenitor-like phenotype, making them an ideal model for functional genomics studies in a hematopoietic lineage context, while also serving as a versatile platform for pathway interrogation.
ARID1B encodes a DNA-binding subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex, which utilizes ATP hydrolysis to reposition nucleosomes and regulate transcription. ARID1B directly interacts with core complex members SMARCA4 (BRG1), SMARCB1, and ARID1A to assemble functional chromatin remodeling modules. Its expression is activated by transcription factors SOX2 and MYC, and it controls a network of downstream targets, including the cell cycle inhibitor CDKN1A, the apoptotic regulators BCL2 and BAX, and neurodevelopmental factors NEUROD1 and TBR1. Through the BAF complex, ARID1B integrates signaling from the Wnt pathway, modulating effectors like CTNNB1, TCF7L2, and GSK3B, and the Notch pathway to orchestrate gene expression programs that balance proliferation, differentiation, and development.
In the HAP1 cellular context, knockout of ARID1B disrupts SWI/SNF complex integrity, leading to aberrant nucleosome positioning and deregulated transcription. The p53-deficient background of HAP1 permits the study of ARID1B’s role in tumor suppression and oncogenesis independently of p53-mediated apoptotic responses. This model is particularly relevant for investigating the molecular mechanisms underlying ARID1B-related neurodevelopmental disorders such as Coffin-Siris syndrome, intellectual disability, and autism spectrum disorder, as well as ARID1B-mutant cancers including ovarian clear cell carcinoma and hepatocellular carcinoma, where SWI/SNF dysfunction contributes to pathogenesis.
These polyclonal knockout cells are suited for a broad range of experimental applications, including chromatin immunoprecipitation (ChIP-qPCR) to probe SWI/SNF complex occupancy at target loci, RNA sequencing to define ARID1B-dependent transcriptomes, and immunofluorescence to visualize complex localization. Functional assays can assess proliferation, apoptosis (via flow cytometry), and drug sensitivity, while western blotting and RT-qPCR validate knockout efficiency and downstream molecular changes. This versatile product supports therapeutic target identification and mechanistic studies in chromatin biology and disease modeling. For further information or to inquire about ordering, please contact Ascent Research.
