The AQP11 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HeLa human cervical adenocarcinoma cell line, featuring targeted disruption of the AQP11 gene. This loss-of-function model enables researchers to investigate the cellular consequences of AQP11 ablation in a well-characterized epithelial cancer background. The polyclonal knockout pool provides a heterogeneous population of edited cells, suitable for functional genomic studies without the selective pressure of single-cell cloning.
HeLa cells are an immortalized human epithelial cell line originally isolated from a cervical adenocarcinoma. They are aneuploid and contain integrated human papillomavirus 18 (HPV-18) sequences, contributing to their robust and rapid proliferation in vitro. Due to their well-documented characteristics, HeLa cells are a staple model in cancer biology, cell signaling, and gene function research, offering a reproducible system for investigating molecular mechanisms.
AQP11 encodes an atypical aquaglyceroporin that resides in the endoplasmic reticulum (ER) membrane, where it facilitates the transport of water and glycerol. This protein is critical for maintaining ER homeostasis, proper protein folding, and trafficking. AQP11 interacts with ER chaperones including SIL1 and BiP/GRP78, and its loss triggers the unfolded protein response (UPR) through activation of ER stress sensors IRE1??, PERK, and ATF6. Downstream signaling cascades lead to transcriptional upregulation of CHOP, splicing of XBP1, and activation of apoptotic executors caspase-3 and caspase-9, thereby linking AQP11 function to ER stress-induced apoptosis.
In the HeLa cellular context, AQP11 knockout compromises ER proteostasis, resulting in accumulation of misfolded proteins and constitutive UPR signaling. This sensitizes the cells to ER stress-mediated apoptosis, making the model valuable for dissecting survival mechanisms in cancer cells that often exhibit heightened basal ER stress. The knockout cells serve as a platform to explore how cervical carcinoma cells regulate the balance between adaptive UPR and pro-apoptotic signaling, potentially informing therapeutic strategies that target the ER stress axis.
This cell population is ideally suited for a range of experiments, including western blot analysis of ER stress markers (GRP78, CHOP), RT-qPCR profiling of UPR target genes, Annexin V-based apoptosis assays, immunofluorescence microscopy of ER morphology, and co-immunoprecipitation studies of AQP11 interactomes. Additionally, it can be employed in drug response studies to evaluate compounds that modulate ER stress or induce apoptosis, such as proteasome inhibitors or BH3 mimetics. For more information, please contact Ascent Research.
