The ATAD2B Knockout HT29 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 human colorectal adenocarcinoma cells, designed to disrupt the ATAD2B gene. This polyclonal pool provides a heterogeneous loss-of-function model, enabling robust functional studies without single-cell cloning artifacts. The knockout strategy broadly targets the ATAD2B locus to abolish its expression, facilitating investigation of its roles in chromatin biology and oncogenic signaling.
HT29 cells are a well-characterized human colorectal adenocarcinoma line isolated from a primary tumor of a 44-year-old female. These cells serve as a standard model for intestinal epithelial biology, including studies of barrier function, differentiation, and colorectal cancer pathogenesis. Their ability to form polarized monolayers and undergo differentiation under specific conditions makes them particularly valuable for examining epithelial homeostasis and transformation mechanisms.
ATAD2B encodes a putative ATPase and chromatin regulator that participates in nuclear receptor-mediated transcription and chromatin dynamics. It functions within key oncogenic networks, acting downstream of MYC and E2F1 and interacting with estrogen receptor alpha (ER??) and BRG1, a component of the SWI/SNF remodeling complex. ATAD2B is implicated in promoting cell proliferation and DNA replication, in part by coregulating targets such as cyclin D1 and ribosomal protein genes. Through associations with histone acetyltransferases like p300, it influences histone H3/H4 acetylation, linking chromatin remodeling to transcriptional control in hormone-responsive and proliferative pathways.
In the HT29 colorectal adenocarcinoma context, ATAD2B disruption is expected to impair chromatin remodeling and nuclear receptor-mediated transcription, potentially attenuating MYC and estrogen receptor signaling pathways critical for tumor cell growth. The loss of ATAD2B may reduce expression of proliferation-associated genes, alter cell cycle progression, and affect differentiation programs. This model thus enables dissection of ATAD2B??s contributions to colorectal cancer biology, including its interplay with the SWI/SNF complex and downstream effectors like cyclin D1.
Researchers can employ this knockout system for a variety of advanced applications, including mechanistic studies of ATAD2B in colorectal cancer, chromatin remodeling assays, and drug target validation. The polyclonal population is compatible with quantitative techniques such as RT-qPCR and western blotting for expression analysis, ChIP-qPCR for chromatin occupancy, and RNA-seq for transcriptome profiling. Functional readouts like MTT or BrdU proliferation assays, colony formation, and flow cytometric cell cycle analysis are readily applicable. Additionally, reporter gene assays can monitor ER?? transcriptional activity, and co-immunoprecipitation can probe protein interactions with factors like MYC or BRG1. This product is ideally suited for synthetic lethal screens and signaling pathway analysis. For further details, please contact Ascent Research.
