The ATAD2 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the ATAD2 gene has been targeted for disruption. This loss-of-function model eliminates ATAD2 protein expression, enabling investigation of its role in chromatin remodeling and nuclear receptor coactivation. The polyclonal format provides a pooled population free of clonal variability, ideally suited for functional genomic studies in a high-transfection-efficiency background.
The host cell line HEK293T is a widely used human embryonic kidney epithelial cell line that stably expresses the SV40 large T-antigen. This feature enhances episomal replication and contributes to its exceptionally high transfection efficiency, making HEK293T a preferred platform for transient and stable expression studies. Its epithelial morphology and rapid growth facilitate large-scale biochemical and cell-based assays, while its non-tumorigenic nature allows study of oncogenic pathways without confounding cancer mutations.
ATAD2 (ATPase family AAA domain-containing protein 2) is a chromatin-remodeling ATPase and transcriptional coactivator for estrogen receptor ?? (ER??) and androgen receptor (AR). It functions downstream of E2F1 and MYC and is induced by estrogen and androgen signaling. ATAD2 binds acetylated histones through its bromodomain, recruits the SWI/SNF complex, and interacts with BRD4 to facilitate expression of cell cycle genes such as CCND1 and CDK1. The ER??-ATAD2-CCND1-CDK4 axis drives hormone-dependent proliferation. CRISPR-mediated knockout disrupts this axis, abolishing ATPase-dependent chromatin remodeling, reducing histone acetylation, and impairing E2F- and steroid hormone-driven transcriptional networks.
In HEK293T cells, ATAD2 knockout provides a clean cellular system to dissect its coactivator functions independently of endogenous steroid receptor activity. These cells can be co-transfected with ER?? or AR and cognate reporters to reconstitute hormone-responsive signaling, allowing direct assessment of ATAD2??s contribution to nuclear receptor transactivation. The polyclonal knockout population is a powerful tool for studying impacts on chromatin dynamics, DNA replication, and cell cycle control in a readily manipulable background, and its high transfection efficiency enables genome-wide CRISPR screens or compound library screening.
This knockout model supports a broad range of cancer research applications, including mechanistic studies in breast cancer, prostate cancer, hepatocellular carcinoma, ovarian cancer, and acute myeloid leukemia. Typical assays include western blotting to confirm ATAD2 depletion, RT-qPCR for downstream targets CCND1 and CDK1, ChIP-qPCR for histone H3 acetylation changes, MTS proliferation assays, luciferase-based reporter assays for ER/AR activity, and flow cytometry for cell cycle analysis. For inhibitor screening, these cells can be used in viability or reporter-based assays to identify compounds that phenocopy ATAD2 loss. For further information, please contact Ascent Research.
