The H2BC18 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-mediated target-gene-disrupted polyclonal population derived from the HeLa cell line. This product comprises a heterogeneous pool of edited cells carrying disruptions in the H2BC18 gene, which encodes a replication-dependent histone H2B variant. As a polyclonal knockout model, it enables functional studies of H2BC18 without clonal selection, preserving population-level genetic diversity and facilitating the investigation of chromatin-related phenotypes in a cancer cell context.
The HeLa host cell line is an immortalized human cervical adenocarcinoma cell line positive for human papillomavirus type 18 (HPV18). These epithelial cells exhibit robust proliferation and are widely used as a model system for cancer biology, signal transduction, and gene regulation. Their transformed phenotype and well-characterized genomic landscape make them a suitable background for dissecting the roles of histone variants in malignant processes.
H2BC18 encodes a canonical histone H2B that is incorporated into nucleosomes during DNA replication. Its expression is tightly controlled by cell-cycle cues, being transcriptionally activated by E2F transcription factors and NPAT upon Cyclin E/CDK2-dependent phosphorylation, while p53 can repress its transcription under stress conditions. The H2B protein forms octameric nucleosome cores with H2A, H3, and H4, and its deposition is facilitated by histone chaperones including NAP1 and the CAF-1 complex. Chromatin remodeling complexes such as SWI/SNF further modulate H2BC18-containing nucleosome accessibility, thereby influencing global gene transcription, DNA repair, and chromatin architecture. Disruption of H2BC18 impairs proper nucleosome assembly, leading to altered chromatin states and potential transcriptional dysregulation.
In the HeLa cervical adenocarcinoma model, knockout of H2BC18 offers insights into how replication-coupled histone supply impacts chromatin integrity and cancer cell phenotypes. Aberrant expression of histones is often associated with tumorigenesis, and H2BC18 loss may mimic conditions of histone deficiency that provoke genomic instability, altered gene silencing, and stress responses. This model is thus valuable for studying the intersection of chromatin dynamics and oncogenic transformation, particularly in HPV-driven cancers.
Researchers can employ this polyclonal knockout population in a variety of assays to assess chromatin structure, gene expression, and cellular functions. Western blotting and immunofluorescence can confirm H2BC18 protein loss, while ChIP-qPCR or ChIP-seq enable mapping of histone modifications and nucleosome positioning. Transcriptional profiling via RNA-seq reveals downstream gene expression changes, and functional assays such as cell cycle analysis, proliferation assays, and Comet assays allow evaluation of growth and DNA damage responses. This product is suitable for applications in chromatin biology, epigenetics, and cancer research. For additional technical information, please contact Ascent Research.
