The ATRAID Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human hepatocellular carcinoma SK-HEP-1 cells carrying a targeted disruption of the ATRAID gene. This product provides a loss-of-function model for investigating the role of ATRAID in retinoic acid signaling, apoptosis, and cell cycle regulation. The polyclonal format represents a heterogeneous mixture of edited cells, ensuring retention of population-level biological complexity while eliminating wild-type ATRAID expression through CRISPR/Cas9-mediated gene disruption.
The SK-HEP-1 host cell line is a well-established adherent epithelial line originally derived from the ascitic fluid of a patient with hepatocellular carcinoma. These cells are widely employed in hepatic cancer research, drug metabolism studies, and toxicology testing, reflecting their ability to form tumors in vivo and to express liver-specific metabolic enzymes. As a model for hepatocellular carcinoma, SK-HEP-1 cells are particularly suited to studies of tumor suppressor gene function and therapeutic responsiveness.
ATRAID encodes a nuclear receptor target protein that is transcriptionally activated by all-trans retinoic acid (ATRA) through retinoic acid receptor (RAR)/retinoid X receptor (RXR) heterodimers. Upon induction, ATRAID promotes intrinsic apoptosis via Bcl-2 family proteins such as BAX and caspase-3 activation, while also enforcing cell cycle arrest through upregulation of the cyclin-dependent kinase inhibitor p21/CDKN1A. Additionally, ATRAID has been implicated in p53-mediated tumor suppression, linking retinoid signaling to canonical cell cycle checkpoints. The protein interacts with RAR/RXR complexes, transcriptional co-regulators, and Bcl-2 family members, positioning it as a nexus between differentiation cues and growth-inhibitory programs.
In the SK-HEP-1 hepatocellular carcinoma context, disruption of ATRAID is expected to impair ATRA-induced apoptosis and differentiation, potentially conferring resistance to retinoid-based therapies and enhancing tumorigenic properties. This knockout model thus enables the interrogation of ATRAID??s tumor suppressor functions and its role in maintaining hepatic epithelial identity. Researchers can use these cells to assess how loss of ATRAID alters signaling through RAR/RXR, p53, and downstream apoptotic effectors, and to explore whether ATRAID loss contributes to the dedifferentiated phenotype characteristic of aggressive hepatocellular carcinoma.
Applications of the ATRAID Knockout SK-HEP-1 Polyclonal Cells encompass detailed mechanistic studies of retinoic acid signaling, phenotypic rescue experiments, and drug-screening campaigns for agents that restore differentiation or induce apoptosis independently of ATRAID. Representative assays include Western blotting and RT-qPCR to confirm ATRAID ablation, Annexin
V/PI flow cytometry for apoptosis quantification, cell cycle analysis to detect G1/S arrest defects, and ATRA dose?Cresponse assays to gauge chemosensitivity. Transcriptomic profiling via RNA-seq can further elucidate the global gene expression changes resulting from ATRAID loss. For additional technical details or to arrange a consultation, please contact Ascent Research.
