The ATXN1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, with disruption of the ATXN1 gene. The polyclonal format provides a heterogeneous pool of genome-edited cells, suitable for functional studies without clonal selection, and is advantageous for population-level analyses such as pooled screening.
HeLa cells are a well-characterized human cervical adenocarcinoma epithelial cell line, positive for HPV18. They are widely used in biomedical research for studies of signal transduction, cancer biology, and gene regulation, offering a robust model for transcriptional and protein interaction analyses.
ATXN1 encodes ataxin-1, a transcriptional regulator involved in RNA splicing and gene repression. It is a core component of the Capicua (CIC)-ATXN1 repressor complex, which directly targets ETV1, ETV4, and ETV5. ATXN1 activity is modulated by AKT1-mediated phosphorylation at S776, promoting interaction with 14-3-3 proteins (YWHAB) and affecting complex dynamics. Additional interactors include RBM17, ATXN1L, NCOR2, and HDAC3, integrating ATXN1 with chromatin remodeling and Notch signaling through CSL/RBPJ. Thus, ATXN1 serves as a hub linking CIC-dependent repression, Notch signaling, and chromatin regulation.
Knockout of ATXN1 in HeLa cells disrupts the CIC-ATXN1 complex, leading to derepression of ETV1/4/5 and other targets. This models loss-of-function aspects of spinocerebellar ataxia type 1 (SCA1), a neurodegenerative disorder. As HeLa cells are non-neuronal, this model enables dissection of fundamental transcriptional and signaling roles of ATXN1 without disease-related aggregation, allowing study of gene expression, Notch pathway, and protein networks in an epithelial context.
This polyclonal knockout cell population supports a wide range of experimental approaches. Researchers can validate ATXN1 disruption using Western blotting and RT-qPCR, and perform RNA-seq to assess global transcriptional changes. ChIP-qPCR can quantify binding of CIC or other factors at target loci. Co-immunoprecipitation and immunofluorescence enable analysis of altered protein interactions and subcellular localization. Reporter assays for CIC and Notch activity provide functional readouts of pathway state. These cells are suitable for drug screening to identify modifiers of ATXN1-related pathways or SCA1 phenotypes. For additional information, please contact Ascent Research.
