Protein folding in the ER is critical for the survival of individual cells. Since secretion underlies multicellularity, the balance of ER protein folding dynamics has a significant impact on mammalian physiology. Dysregulation of endoplasmic reticulum homeostasis can lead to chronic diseases in humans. Therefore, it is important to use mammalian cells to study ER stress and UPR to understand UPR and ER stress-related diseases.
Fig. 1 Response categories of the Unfolded Protein Response (Oslowski et al., 2011)
Creative Bioarray has established a platform based on cell culture systems and endoplasmic reticulum stress induction techniques. In this endoplasmic reticulum stress induction platform, we have judged and screened several mammalian cell lines that are responsive to commonly used ER stress inducers and subsequent UPR activation. In addition, we have a variety of commonly used endoplasmic reticulum stress inducers, including pharmacological ER stress inducers and physiological ER stress inducers.
UPR is particularly important for maintaining ER homeostasis in specialized secretory cells, such as pancreatic β-cells and plasma cells. Mouse embryonic fibroblasts (MEF) are a powerful tool for studying UPR. We can provide customers with MEFs from Ire1α, Ire1β, Perk, ATf6α, ATF6β, Xbp-1, Atf4, and Gadd34 knockout mice.
UPR is particularly important for maintaining ER homeostasis in specialized secretory cells, such as pancreatic β cells and plasma cells. We offer mouse β-cell lines and rat β-cell lines that can be used to study ER stress and UPR in a β-cell context.
The compounds we use to induce ER stress and activate UPR in tissue culture systems include clathrin, toxic carotene, Brefeldin A, dithiothreitol (DTT), and MG132.
We will determine the therapeutic concentration and duration of ER stress induction by these compounds for each specific system. It usually takes only a few hours to induce ER stress, and prolonged exposure usually induces ER stress-mediated cell death.
Physiological disruptors are commonly used to induce mild ER stress in tissue culture systems. The amount and duration of exposure to these inducers should be determined in a given system, as described for drug inducers.
Glucose deprivation prevents N-linked glycosylation and reduces cellular ATP levels, leading to ER stress in many cell types. Endoplasmic reticulum stress can be induced by treating cells with a glucose-free medium for 24-48 hours.
ER stress and UPR are unique among cells. Therefore, for a given cell type, there are specific ER stress inducers, each of which activates UPR differently.
Creative Bioarray is dedicated to providing high-quality products, comprehensive services, and tailored solutions to support and facilitate life sciences and pharmaceutical research and development. If you have any questions or needs, please contact us, and our customer service staff will help you the first time.