The DNTTIP1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DNTTIP1 gene. This heterogeneous pool of cells carries CRISPR/Cas9-mediated gene edits, enabling functional studies without clonal isolation. The polyclonal format ensures effective knockout across the population and is suitable for diverse downstream assays.
The host HeLa cell line is a human epithelial cervical carcinoma line derived from a cervical adenocarcinoma (Henrietta Lacks, 1951). These immortalized, HPV18-positive cells are a cornerstone of cancer research, providing a physiologically relevant model for studying oncogenic transformation and viral pathogenesis.
DNTTIP1 (TdIF2) interacts with terminal deoxynucleotidyltransferase (TdT) to modulate DNA polymerase activity during V(D)J recombination. It also associates with histone deacetylase complexes containing HDAC1, HDAC2, and the NuRD complex subunit MTA2, mediating transcriptional repression and chromatin remodeling. Key pathway components include TdT, HDAC1, HDAC2, MTA2, CHD4, RAG1, and RAG2, highlighting DNTTIP1’s role at the interface of DNA repair and epigenetic control.
In HeLa cells, DNTTIP1 knockout offers insight into epigenetic dysregulation in cervical carcinoma. HPV18 oncoproteins manipulate host chromatin regulators, so loss of DNTTIP1 may alter HDAC complex function and transcriptional programs. This model thus enables studies of viral oncoprotein-host epigenetic interactions and broader cancer-related chromatin remodeling.
These polyclonal knockout cells are ideal for RNA-seq to identify DNTTIP1-dependent transcriptomic changes, ChIP-qPCR for assessing histone modifications, reporter gene assays to measure transcriptional activity, and western blotting or RT-qPCR for confirmation of gene disruption. Migration and invasion assays can further evaluate effects on cancer cell behavior. For further information, contact Ascent Research.
