H2BC17 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population engineered to disrupt the H2BC17 gene in the HeLa host cell line. This product consists of a heterogeneous pool of cells carrying targeted disruptions in the endogenous H2BC17 locus, leading to loss of histone H2B protein function. The polyclonal format ensures a diverse representation of gene-edited alleles, making it a versatile model for studying the consequences of H2BC17 deficiency without clonal selection bias. This knockout tool is intended for use in cell biology, cancer research, and epigenetics.
The host cell line, HeLa, is an immortalized cervical adenocarcinoma epithelial cell line derived from the tumor of Henrietta Lacks. These cells are HPV18-positive and retain features of epithelial barrier function and secretory capacity. HeLa cells are one of the most widely employed models in biomedical research, with applications spanning cancer biology, signal transduction, and drug discovery. Their robust growth characteristics and well-characterized genomic landscape make them an ideal platform for generating knockout models to study gene function.
H2BC17 encodes histone H2B, a core nucleosome component essential for chromatin architecture. It forms an octamer with H2A, H3, and H4, assembled by chaperones NAP1 and FACT. Expression is cell-cycle-regulated by E2F, NPAT, Cyclin E/CDK2, and Oct-1. Loss of H2B disrupts nucleosome stability, impairing DNA replication, repair, condensation, and transcription. Chromatin remodelers like SWI/SNF and histone-modifying enzymes require intact H2B for activity.
In the HeLa cervical adenocarcinoma background, H2BC17 knockout provides a system to investigate histone-driven epigenetic dysregulation linked to tumorigenesis. HeLa cells express HPV18 E6 and E7 oncoproteins that subvert p53 and Rb pathways, and their chromatin landscape is affected; therefore, ablating a core histone like H2B may reveal unique vulnerabilities or altered epigenetic dependencies. The resulting destabilization of chromatin is expected to impair DNA replication, repair, and cell cycle progression, potentially influencing cancer cell proliferation and survival. This model is valuable for studying histone mutations in cancer, chromatinopathies, and epigenetic regulation within a well-established malignant epithelial context.
This polyclonal knockout population is suitable for epigenetics, chromatin biology, and cancer cell biology research. Key techniques include ATAC-seq for genome-wide chromatin accessibility profiling, nucleosome positioning analysis by MNase-seq, and RNA-seq to define transcriptional changes. Cell cycle distribution can be assessed by flow cytometry, and proliferation rates measured via growth curves. Immunofluorescence with antibodies against modified histones reveals epigenetic alterations, while Western blot and RT-qPCR confirm H2BC17 gene disruption. The model supports functional genomics and screening of chromatin-targeted therapeutics. For further information, please contact Ascent Research.
