DNPH1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the DNPH1 gene. This heterogeneous pool of edited HeLa cells provides a loss-of-function model for investigating DNPH1-dependent cellular processes. The product is designed for researchers studying nucleotide metabolism, DNA repair, and c-Myc-driven oncogenesis, enabling analysis of gene disruption effects without the selection of a single clonal isolate.
The host cell line, HeLa, is an HPV18-positive human cervical adenocarcinoma epithelial cell line widely used in cancer research. Its robust growth characteristics, well-characterized genome, and extensive historical use make it an ideal background for studying oncogenic signaling and metabolic reprogramming. The HeLa model offers a relevant context for examining how perturbations in nucleotide salvage pathways influence tumor cell biology.
DNPH1 functions as a deoxynucleoside monophosphate hydrolase, catalyzing the conversion of deoxynucleoside monophosphates to free nucleobases and deoxyribose phosphate. It is transcriptionally regulated by the c-Myc oncoprotein, linking nucleotide metabolism to c-Myc-driven proliferation. DNPH1 contributes to nucleotide salvage and maintenance of dNTP pools, implicating it in DNA replication fidelity and repair. Downstream, its enzymatic activity generates free nucleobases and influences nucleotide pool composition, potentially impacting DNA repair intermediates.
In HeLa cells, where c-Myc is often dysregulated, DNPH1 knockout allows dissection of how this target gene supports oncogenic metabolic adaptation. Loss of DNPH1 may alter nucleotide homeostasis and DNA damage responses, providing a platform to study mechanisms that sustain rapid proliferation. This polyclonal population enables assessment of functional consequences in a heterogeneous cancer cell background, reflecting the complexity of tumor cell populations.
Typical applications include Western blotting to confirm DNPH1 disruption, enzyme activity assays measuring nucleoside monophosphate hydrolysis, and nucleotide pool quantification by LC-MS. Researchers can employ clonogenic survival assays following DNA-damaging agents to evaluate repair capacity, and qPCR to monitor expression of downstream c-Myc targets. This model is suited for investigating c-Myc-driven oncogenesis, nucleotide metabolism, and drug targeting strategies. For further information, please contact Ascent Research.
