The DZIP3 Knockout HeLa Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population in which the human DZIP3 gene has been disrupted. This product provides a heterogeneous HeLa cell pool bearing diverse gene-disruption events, enabling loss-of-function studies without clonal selection. As a polyclonal knockout model, it circumvents clonal artifacts and preserves cellular heterogeneity inherent to tumor populations. The knockout is generated using CRISPR/Cas9-mediated genome editing, leading to stable DZIP3 disruption; the polyclonal format supports robust and reproducible experiments when working with bulk cellular phenotypes.
HeLa cells are an immortalized human cell line derived from cervical adenocarcinoma epithelial tissue and harbor integrated human papillomavirus type 18 (HPV-18) sequences. As one of the most widely used cancer cell lines, HeLa offers a well-characterized model for studying cell cycle regulation, signal transduction, and oncogenic processes. Their robust growth, ease of manipulation, and extensive molecular characterization make them an ideal host for dissecting gene function in a cancer-relevant context. The DZIP3 knockout in this background permits the interrogation of ubiquitin-mediated pathways within a system that retains key transformation features.
DZIP3 encodes an E3 ubiquitin-protein ligase that catalyzes the transfer of ubiquitin to substrate proteins, regulating their stability, localization, or activity. DZIP3 is implicated in RNA metabolism and stress granule dynamics, likely by targeting specific RNA-binding proteins for ubiquitination. It operates downstream of cellular stress signals such as oxidative stress and heat shock, and interacts with proteins including DAZ, DAZL, PABPC1, and other stress granule constituents. Through these interactions, DZIP3 modulates the assembly and disassembly of stress granules, thereby influencing the cellular response to adverse conditions. Representative pathway components include ubiquitin, the proteasome, RNA-binding proteins, and stress granule scaffolds, positioning DZIP3 at a regulatory nexus between proteostasis and RNA biology.
In the HeLa cancer-cell context, DZIP3 disruption offers a unique system to explore how E3 ligase activity impacts stress adaptation mechanisms relevant to cancer cell survival. Stress granules are often dysregulated in cancer, and their formation can promote resistance to chemotherapy and other cellular insults. By eliminating DZIP3 function, researchers can dissect the ubiquitination events that govern stress granule dynamics and RNA fate in a model of human carcinoma. Moreover, DZIP3??s interaction with DAZ family proteins, which are critical in spermatogenesis, expands the model??s utility to infertility research, as HeLa cells provide a convenient platform for studying conserved RNA-regulatory complexes.
This DZIP3 knockout cell pool is suitable for a broad range of research applications, including ubiquitination pathway analysis via western blotting for target ubiquitination, stress granule visualization by immunofluorescence, co-immunoprecipitation to map DZIP3 interactomes, and RT-qPCR for stress-responsive transcripts. The polyclonal nature allows assessment of population-level responses to stress, drug treatments, or genetic complementation. These cells support investigations into cancer cell biology, RNA metabolism, and the molecular basis of male infertility. For detailed technical inquiries or customization requests, please contact Ascent Research.
