The H2AC11 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the H2AC11 gene in HeLa cells. This loss-of-function model enables investigation of the replication-dependent histone H2A variant, a critical nucleosome component. The polyclonal format prevents clonal bias and captures population-level chromatin responses, making it ideal for functional genomics and epigenetic studies. These cells are supplied ready-to-use for immediate experimentation, providing a reliable tool for dissecting H2A variant biology across diverse research applications.
The HeLa host cell line is an immortalized cervical adenocarcinoma model established from Henrietta Lacks in 1951. These HPV18-positive, aneuploid epithelial cells are extensively utilized in biomedical research due to their rapid growth and well-characterized biology. HeLa??s genetic tractability and clinical relevance to cervical cancer make it an ideal platform for CRISPR-edited knockout populations studying chromatin-related oncogenic mechanisms. The cell line??s widespread adoption provides a solid foundation for functional genomics and epigenetic investigations.
H2AC11 encodes a replication-dependent histone H2A variant that assembles into nucleosomes with H2B, H3, and H4. Its expression is orchestrated by E2F transcription factors, Cyclin E/CDK2 kinase activity, and NPAT, with p53-mediated repression under stress. The H2A variant interacts with histone chaperones NAP1 and FACT, and its chromatin deposition requires ASF1 and CAF-1. Once incorporated, the nucleosomes are remodeled by SWI/SNF, modulating chromatin architecture, gene expression programs, and DNA replication fidelity. CRISPR/Cas9-mediated knockout of H2AC11 eliminates this central histone component, disrupting nucleosome assembly and provoking epigenetic instability and potential defects in cell cycle progression.
In HeLa cervical carcinoma cells, H2AC11 knockout offers a powerful model for studying chromatin-driven oncogenic mechanisms. The HPV18-positive, aneuploid background may reveal synthetic lethalities or altered drug sensitivities stemming from histone variant loss, with implications for cervical cancer and chromatinopathies. The polyclonal population mirrors tumor heterogeneity, enabling robust analysis of H2A variant function in cell cycle control, DNA damage repair, and epigenetic therapy response. This system helps dissect replication-dependent histone roles in genomic stability.
Researchers can employ this knockout population in a variety of assays, including ChIP-qPCR, Western blotting, RT-qPCR, immunofluorescence, and flow cytometry for cell cycle profiling. Proliferation assays, DNA damage response measurements, and transcriptomic analyses via RNA-seq are readily applicable. The model supports investigations in histone biology, chromatin dynamics, cancer epigenetics, and drug sensitivity screening. For technical support and detailed experimental guidance, please contact Ascent Research.
