The HDAC1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the HeLa human cervical adenocarcinoma line, with targeted disruption of the HDAC1 gene. This heterogeneous pool enables loss-of-function studies of histone deacetylase 1 in an HPV18-positive epithelial model, providing a tool to explore epigenetic regulation and chromatin remodeling.
The parental HeLa cell line is an immortalized, HPV18-positive cervical cancer-derived epithelial model commonly used in biomedical research. Its well-characterized molecular background and robust growth make it suitable for investigating viral oncoprotein interactions with host epigenetic machinery, and the HDAC1 knockout allows focused dissection of deacetylase-dependent pathways.
HDAC1 catalyzes deacetylation of lysine residues on histone H3 (K9, K14, K18, K23) and H4 (K5, K8, K12, K16) as well as transcription factors p53, E2F1, and SP1, promoting chromatin compaction and transcriptional repression. It functions in corepressor complexes SIN3A, NuRD (CHD4, MBD2, MTA1), and CoREST (RCOR1, LSD1), interacting with proteins such as Rb. Upstream regulation occurs via MYC and p53, with modulation by CK2 phosphorylation. HDAC1 influences pathways including Notch (NICD, RBPJ), Wnt/??-catenin (??-catenin, TCF7L2), TGF-?? (SMAD2/3), and p53, and directly targets CDKN1A (p21), linking epigenetic control to cell cycle and apoptosis.
In HeLa cells, HDAC1 loss disrupts these networks, enabling examination of deacetylase-dependent proliferation, survival, and drug responses within a cervical cancer context. The HPV18-positive background provides insight into viral oncoprotein?CHDAC interplay. The polyclonal nature captures population-level phenotypic diversity, avoiding clonal bias and facilitating robust assessment of epigenetic interventions and drug sensitivity.
This product supports diverse applications: Western blotting and immunofluorescence to confirm HDAC1 ablation and global histone acetylation changes; RT-qPCR and RNA-seq for transcriptomic profiling; ChIP-qPCR for locus-specific histone modification analysis; flow cytometry for cell cycle and apoptosis evaluation; and HDAC activity assays. It is particularly useful for testing HDAC inhibitors like vorinostat and trichostatin A, enabling compound screening in an HDAC1-deficient background. For further details, please contact Ascent Research.
