ATXN7L2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the widely utilized HEK293T human embryonic kidney epithelial cell line. This product introduces a targeted disruption of the ATXN7L2 gene, generating a loss-of-function model that eliminates functional ATXN7L2 protein expression within the polyclonal cell pool. As a component of the SAGA (Spt-Ada-Gcn5 acetyltransferase) transcriptional coactivator complex, ATXN7L2 participates in histone H2B deubiquitination, making this knockout model invaluable for elucidating the molecular mechanisms of transcriptional regulation and chromatin dynamics.
The HEK293T host cell line is a derivative of the HEK293 line, originally established from human embryonic kidney cells immortalized by sheared adenovirus type 5 DNA. HEK293T cells stably express the SV40 large T antigen, which promotes episomal replication of plasmids containing the SV40 origin of replication, thereby enabling high-level transient protein expression and efficient viral packaging for lentiviral and retroviral production. Their robust growth characteristics, ease of transfection, and human epithelial origin make HEK293T cells a preferred model system for molecular and cellular biology studies, including investigations of gene regulation, signal transduction, and cancer-relevant pathways.
ATXN7L2 is a core component of the SAGA complex’s deubiquitinase module (DUBm), interacting with USP22, ATXN7L3, and ENY2 to remove monoubiquitin from histone H2B (H2Bub1). This activity is crucial for transcription elongation and gene activation downstream of transcription factors like MYC and p53, which recruit SAGA to chromatin. By modulating H2B ubiquitination levels, ATXN7L2 influences chromatin structure and transcriptional outputs of genes involved in proliferation, differentiation, and stress responses. Disruption of ATXN7L2 impairs SAGA DUBm function, leading to altered histone modifications and dysregulated gene expression programs linked to cancer and potentially neurodegenerative disorders.
In the HEK293T background, ATXN7L2 knockout enables dissection of SAGA complex-dependent transcriptional regulation in a human epithelial context. The absence of ATXN7L2 allows examination of the SAGA DUBm’s specific contributions to histone modification dynamics and gene expression. HEK293T cells serve as a robust platform for benchmarking transcriptional and signaling assays, making this knockout population ideal for comparative studies of SAGA subunit functions. This model is particularly suited to explore how ATXN7L2-mediated H2B deubiquitination intersects with pathways governed by oncogenic transcription factors, offering insights into cancer biology and therapeutic targets.
This polyclonal knockout cell population is designed for a broad range of functional assays, including Western blotting for detecting global H2B ubiquitination changes, RT-qPCR for quantifying target gene expression, co-immunoprecipitation to assess SAGA complex integrity, ChIP-qPCR to map histone modification alterations at specific loci, and RNA-seq for transcriptomic profiling. These applications enable rigorous dissection of ATXN7L2-dependent transcriptional networks and their implications in cancer and neurodegeneration. For further information, please contact Ascent Research.
