The H2AC25 Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population featuring targeted disruption of the human H2AC25 gene, which encodes a canonical histone H2A protein. This loss-of-function model was generated in HeLa cells and is delivered as a polyclonal knockout product, providing a heterogeneous population of cells with H2AC25 gene disruption. The absence of functional H2AC25 protein disrupts nucleosome stoichiometry, making this model suitable for investigating chromatin-based regulatory mechanisms.
The host HeLa cell line is an epithelial cell line derived from HPV18-positive cervical adenocarcinoma. These cells are widely employed in cancer research, as they carry integrated human papillomavirus oncogenes that perturb cell cycle regulation. The HeLa epigenetic landscape is notably susceptible to alterations in histone dynamics, rendering it an ideal platform for studying histone-coding gene function. The HPV18 E6 and E7 oncoproteins modulate p53 and Rb pathways, contributing to chromosomal instability and altered gene expression profiles that intersect with chromatin organization.
H2AC25 is a core component of histone octamers, forming nucleosomes with histone H2B, H3, and H4 to package genomic DNA. The expression of H2AC25 is transcriptionally regulated by the cyclin E/CDK2 axis through the E2F and NPAT activators, with HINFP serving as a cofactor. The translated H2A protein interacts with histone chaperones such as NAP1 and the FACT complex during nucleosome assembly and is subject to rearrangement by chromatin remodelers. Downstream, functional nucleosome arrays mediate transcriptional regulation of target genes and facilitate the DNA damage response. Disruption of H2AC25 therefore impairs these higher-order chromatin functions.
In HeLa cells, knockout of H2AC25 provides a unique model to examine how altered nucleosome composition influences oncogenic chromatin states. Given the role of canonical histones in maintaining epigenetic memory and genome integrity, H2AC25 loss can affect cell cycle progression, DNA repair efficiency, and transcriptional programs. This model is particularly relevant for studying epigenetic dysregulation in cervical cancer, where aberrant chromatin organization contributes to tumorigenesis. By perturbing histone stoichiometry, researchers can dissect the interplay between histone supply and cancer cell proliferation.
This polyclonal knockout product supports a range of experimental applications, including western blotting and RT-qPCR to confirm H2AC25 depletion, chromatin immunoprecipitation (ChIP) to assess histone modifications, and immunofluorescence to visualize chromatin architecture. Functional studies may utilize cell cycle analysis by flow cytometry, RNA-seq for transcriptome profiling, ATAC-seq for chromatin accessibility, and apoptosis assays under genotoxic stress. These approaches enable investigation of histone H2A function in chromatin organization and its role in cervical cancer biology. For further information or technical inquiries, please contact Ascent Research.
