The ATF6B Knockout HeLa Polyclonal Cells product is a population of HeLa cells that have been subjected to CRISPR/Cas9-mediated gene editing to disrupt the ATF6B locus. As a polyclonal knockout pool, it provides a heterogeneous loss-of-function model without single-cell cloning, enabling studies that rely on population-level phenotypes. This format is particularly useful for analyzing ATF6B??s role in the regulation of ER homeostasis and the unfolded protein response.
The HeLa cell line is a human epithelial cell line derived from an HPV18-positive cervical adenocarcinoma, widely used as a model in cancer research. Its transformed state, rapid growth, and thoroughly characterized signal transduction networks make it an ideal host for studying cellular stress adaptation. The epithelial origin provides a relevant context for investigating how ATF6B-dependent pathways contribute to tumor cell survival under adverse conditions.
ATF6B is an ER transmembrane transcription factor that serves as a stress sensor in the UPR. Upon ER stress induced by stimuli like tunicamycin or thapsigargin, ATF6B traffics to the Golgi, where regulated intramembrane proteolysis releases its N-terminal fragment. This active fragment enters the nucleus and, in concert with ATF6 and XBP1, activates transcription of chaperones such as HSPA5 (BiP) and HSP90B1, as well as ER-associated degradation components, thus restoring proteostasis. ATF6B functions within a network that includes IRE1/ERN1 and PERK/EIF2AK3, and is negatively regulated by BiP under non-stress conditions.
In HeLa cells, ATF6B knockout allows investigation of the ATF6 arm of the UPR in a cancer-relevant background. HeLa cells depend on efficient ER stress responses to cope with high secretory demands and the metabolic stress of rapid proliferation. Disruption of ATF6B may impair the ability to resolve ER stress, potentially leading to increased sensitivity to pro-apoptotic signals. This model is thus valuable for identifying vulnerabilities in tumor cells and for studying the interplay between UPR signaling and oncogenic pathways such as those driven by HPV18 E6/E7.
This polyclonal knockout product supports diverse research applications, including western blot analysis of ATF6B cleavage, RT-qPCR profiling of UPR target genes, immunofluorescence imaging of ATF6B subcellular localization, and cell viability assays under ER stress conditions induced by pharmacological agents. It can also be used in drug screening campaigns aimed at discovering small-molecule modulators of the UPR, and in flow cytometry to monitor ER stress markers. The population-level knockout is particularly suited for experiments where clonal artifacts are undesirable. For further technical details, contact Ascent Research.
