ATAD2B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 human hepatic adenocarcinoma line. These cells carry a targeted disruption of the ATAD2B gene, which encodes a bromodomain-containing AAA ATPase involved in chromatin remodeling and transcriptional regulation. The polyclonal format provides a heterogeneous knockout pool ideal for loss-of-function studies without clonal bias. This product serves as a robust model for investigating hepatocellular carcinoma biology and epigenetic control of gene expression.
SK-HEP-1 is a hepatic adenocarcinoma cell line established from ascites fluid of a liver cancer patient. It exhibits epithelial morphology and characteristic genomic alterations of hepatocellular carcinoma, including dysregulated MYC and E2F1 signaling. This cell line displays aggressive proliferation and invasive capacity, making it a relevant model for studying liver cancer biology and oncogenic mechanisms. Its genetic background provides a suitable context for examining ATAD2B function in a cancer-relevant setting.
ATAD2B functions as a chromatin-remodeling AAA ATPase that interacts with histones and nucleosome remodeling complexes through its bromodomain. Transcriptionally activated by E2F1 and MYC, it regulates expression of cell cycle genes and proliferation markers. ATAD2B cooperates with BRD proteins and other chromatin modifiers to facilitate nucleosome repositioning and transcriptional control. Loss of ATAD2B disrupts these interactions, impairing epigenetic gene regulation and genomic stability.
In the SK-HEP-1 context, ATAD2B knockout is anticipated to attenuate oncogenic transcriptional programs driven by E2F1 and MYC, leading to reduced proliferation, impaired cell cycle progression, and increased susceptibility to genomic instability. This model enables dissection of ATAD2B-dependent pathways in hepatocellular carcinoma. The polyclonal knockout population also permits exploration of clonal heterogeneity in response to ATAD2B depletion.
This knockout model is suitable for western blotting and RT-qPCR to confirm ATAD2B loss, cell proliferation and colony formation assays, flow cytometry for cell cycle analysis, and transwell invasion assays. ChIP-qPCR can be used to examine histone modification changes. It is applicable to functional genomics, cancer epigenetics, and drug discovery targeting chromatin regulators. For additional information or technical support, please contact Ascent Research.
