The AQP11 Knockout HEK293T Polyclonal Cells represent a polyclonal population of HEK293T cells engineered via CRISPR/Cas9-mediated disruption of the AQP11 gene. This product provides a heterogeneous knockout model for studying loss-of-function effects of aquaporin-11 in a human embryonic kidney epithelial background. The polyclonal format preserves a range of editing outcomes, enabling robust analysis of AQP11-dependent cellular phenotypes without the selection bias of clonal isolates. These cells serve as a versatile tool for interrogating endoplasmic reticulum (ER) homeostasis and stress signaling pathways.
HEK293T cells are derived from human embryonic kidney 293 cells by stable integration of the SV40 large T antigen, which enhances episomal replication of transfected plasmids and supports high-level recombinant protein production. These adherent epithelial cells are widely employed for transient and stable protein expression, lentiviral and retroviral packaging, and various genetic manipulation experiments. The kidney epithelial lineage makes HEK293T cells particularly relevant for modeling renal cell biology and disorders affecting renal tubular function, such as polycystic kidney disease and ER stress-related nephropathies.
Aquaporin-11 (AQP11) is an endoplasmic reticulum-resident aquaglyceroporin that facilitates transmembrane water and glycerol transport, critical for maintaining ER luminal volume and preventing protein misfolding. Loss of AQP11 function leads to ER volume expansion and accumulation of unfolded proteins, which activate the unfolded protein response (UPR). Mechanistically, ER stress sensors IRE1, PERK, and ATF6 detect luminal perturbations and trigger downstream signaling. The UPR branches converge on transcription factors ATF4 and XBP1, which drive expression of chaperones like BiP and pro-apoptotic effectors such as CHOP. Sustained UPR activation tips the balance toward apoptosis through modulation of BCL2 family members (BAX, BCL2), recapitulating cellular defects observed in autosomal recessive polycystic kidney disease.
In the HEK293T epithelial context, AQP11 knockout provides a physiologically relevant platform for dissecting ER stress signaling in kidney cells. HEK293T cells express the molecular machinery of the UPR and respond to ER stress with characteristic activation patterns, making them suitable for mechanistic studies. The loss of AQP11 in these cells engenders chronic ER stress and heightened susceptibility to apoptotic stimuli, mirroring pathogenic features of ER stress-associated nephropathies. Researchers can exploit this model to investigate hypertonicity-induced stress responses and the interplay between aquaporin-mediated transport and organelle homeostasis.
Research applications include quantitative Western blotting for AQP11 and UPR markers (p-eIF2??, ATF4, CHOP), RT-qPCR analysis of ER stress target genes (XBP1, BiP, CHOP), immunofluorescence microscopy to visualize ER morphology changes, Annexin V apoptosis assays, and cell viability assessments under stress conditions. This polyclonal knockout pool is well-suited for chemical biology screens of UPR modulators and chemical chaperones aimed at restoring ER function. For further details or technical support, please contact Ascent Research.
