mProX™ Human GIPR Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 The heightened insensitivity observed in the E45Q variant of GIPR results from a diminished exocytosis response following exposure to GIP.
Adipocytes electroporated with WT or E354Q GIPR were serum starved and incubated without or with 100 nM GIP for 1h. The cells were then incubated with anti-HA antibodies for the indicated time points, fixed, permeabilized, and stained with anti-mose Cy3 antibodies. Cell-associated anti-HA (Cy3 fluorescence) normalized to GFP is plotted as a function of incubation time. The slope is proportional to the rate of GIPR internalization.
Ref: Mohammad, Sameer, et al. "A naturally occurring GIP receptor variant undergoes enhanced agonist-induced desensitization, which impairs GIP control of adipose insulin sensitivity." Molecular and cellular biology 34.19 (2014): 3618-3629.
Pubmed: 25047836
DOI: 10.1128/MCB.00256-14
Research Highlights
Zhao F, et al. "Molecular basis of signal transduction mediated by the human GIPR splice ." Proceedings of the National Academy of Sciences of the United States of America, 2023.
The potential drug target, Glucose-dependent insulinotropic polypeptide receptor (GIPR), plays a crucial role in maintaining glucose homeostasis in humans by working with glucagon-like peptide-1 receptor and glucagon receptor. The receptor has been found to have at least 13 splice variants (SVs), with over half exhibiting sequence variations at either the C or N terminus. To gain insight into the role of these variants in GIPR signaling, two N terminus-altered SVs (GIPR-202 and GIPR-209) were studied through cryoelectron microscopy (cryo-EM) structures. It was discovered that these variants do not bind to the hormone or trigger signal transduction, but rather suppress ligand binding and cAMP accumulation of GIPR. Furthermore, one variant (SV1) was found to inhibit beta-arrestin 2 responses. The SV1 and SV2 structures revealed changes in the extracellular halves of transmembrane helices and loops, resulting in a loss of peptide binding ability. These findings suggest a constitutive and ligand-independent form of signal bias, expanding our understanding of biased signaling.
Pubmed:
37792509
DOI:
10.1073/pnas.2306145120
Folli F, et al. "Mechanisms of action of incretin receptor based dual- and tri-agonists in ." American journal of physiology. Endocrinology and metabolism, 2023.
The simultaneous activation of incretin G protein coupled receptors using unimolecular dual-receptor agonists (UDRA) has recently been recognized as a potential treatment option for type 2 diabetes. Additionally, there is a growing interest in the use of triple agonists which can also bind to the glucagon receptor. This scoping review examines the mechanisms of action behind these novel and important classes of peptide receptor agonists. Clinical studies have shown positive outcomes for UDRAs as both monotherapies and when combined with other hypoglycemic treatments. While the combined effects of GLP-1R and GIPR agonism were expected, the additional benefits from GCGR were unexpected. However, the potential for synergistic or antagonistic interactions among these G-protein receptor pathways is not fully understood and requires further investigation. A comprehensive understanding of the cellular mechanisms of action is necessary in order to fully grasp the long-term effectiveness and safety of these therapies.
Pubmed:
37729025
DOI:
10.1152/ajpendo.00236.2023