The ATXN2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by disruption of the human ATXN2 gene in HeLa cells. This product provides a loss-of-function model to investigate ATXN2-dependent molecular pathways. The polyclonal format captures diverse editing outcomes, enabling robust functional studies without the clonal selection bottlenecks inherent to single-cell-derived lines.
HeLa cells are an immortalized human cervical adenocarcinoma cell line of epithelial origin, harboring HPV18 sequences. Widely used in cell biology, HeLa cells offer a consistent and well-characterized background for gene knockout studies, particularly for probing mechanisms of RNA metabolism, stress responses, and signaling pathways relevant to both cancer and neurodegenerative disease contexts.
ATXN2 encodes an RNA-binding protein that regulates mRNA translation and stress granule dynamics through its interactions with PABPC1, G3BP1, TDP-43, and the Lsm1-7 complex. Under cellular stress, ATXN2 is recruited to stress granules via eIF2?? kinase signaling, where it modulates mRNA translation. The protein is also implicated in mTORC1-regulated translation control, and its expanded polyglutamine tract drives aberrant aggregation in spinocerebellar ataxia type 2 (SCA2). ATXN2 furthermore modifies TDP-43 aggregation in amyotrophic lateral sclerosis (ALS), positioning it at the nexus of neurodegeneration-associated proteinopathies.
In the HeLa epithelial context, ATXN2 knockout allows dissection of stress granule biology and RNA processing independently of neuronal-specific factors. Because HeLa cells exhibit robust stress response pathways, they are an ideal platform for examining how loss of ATXN2 alters stress-induced assembly of G3BP1- and PABPC1-positive granules, mTORC1 signaling dynamics, and the translation of specific target mRNAs. This model can reveal epithelial cell-autonomous functions of ATXN2 that may contribute to cancer cell adaptation or drug resistance under stress.
Typical research applications include immunofluorescence staining of stress granule markers (G3BP1, PABPC1) under sodium arsenite?Cinduced stress, western blotting for ATXN2 interactors, co-immunoprecipitation of ATXN2 complexes, and transcriptome-wide analysis by RNA-seq to identify translationally regulated targets. Additionally, these cells enable quantitative stress granule assembly assays and co-immunoprecipitation of ATXN2 interacting partners, facilitating detailed mechanistic studies. The knockout cells are suitable for drug screening campaigns aimed at modulating stress granule formation or ATXN2-associated toxic aggregation. For further technical details and batch-specific performance, please contact Ascent Research.
