ArticleBiochimica et biophysica acta2011
Modulation of α(2C) adrenergic receptor temperature-sensitive trafficking by HSP90.
Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
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- Expression of soluble guanylate cyclase (sGC) and its ability to form a functional heterodimer are crucial for reviving the NO-sGC signaling in PAH.Free radical biology & medicine · 2024Article
- Targeting trafficking as a therapeutic avenue for misfolded GPCRs leading to endocrine diseases.Frontiers in endocrinology · 2022Review
- Misfolded G Protein-Coupled Receptors and Endocrine Disease. Molecular Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2021Review
- Functional characterization of a loss-of-function mutant I324M of arginine vasopressin receptor 2 in X-linked nephrogenic diabetes insipidus.Scientific reports · 2021Article
- Relax, Cool Down and Scaffold: How to Restore Surface Expression of Folding-Deficient Mutant GPCRs and SLC6 Transporters.International journal of molecular sciences · 2017Review
- Hyponatremia and V2 vasopressin receptor upregulation: a result of HSP90 inhibition.Cancer chemotherapy and pharmacology · 2017Article
- Regulation of GPCR expression through an interaction with CCT7, a subunit of the CCT/TRiC complex.Molecular biology of the cell · 2016Article
- Hair cell synaptic dysfunction, auditory fatigue and thermal sensitivity in otoferlin Ile515Thr mutants.The EMBO journal · 2016Article
- Molecular determinants of the human α2C-adrenergic receptor temperature-sensitive intracellular traffic.Molecular pharmacology · 2015Article
- Chaperoning G protein-coupled receptors: from cell biology to therapeutics.Endocrine reviews · 2014Review
- Common α2A and α2C adrenergic receptor polymorphisms do not affect plasma membrane trafficking.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- A G protein-coupled receptor and the intracellular synthase of its agonist functionally cooperate.The Journal of cell biology · 2014Article
- The C-terminal half of the α2C-adrenoceptor determines the receptor's membrane expression level and drug selectivity.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Differential regulation of nitric oxide synthase function in aorta and tail artery from 5/6 nephrectomized rats.Physiological reports · 2013Article
- Δ9-THC increases endogenous AHA1 expression in rat cerebellum and may modulate CB1 receptor function during chronic use.Journal of neurochemistry · 2011Article
- Intracellular α(2C)-adrenoceptors: storage depot, stunted development or signaling domain?Biochimica et biophysica acta · 2011Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Decreasing the temperature to 30°C is accompanied by significant enhancement of α(2C)-AR plasma membrane levels in several cell lines with fibroblast phenotype, as demonstrated by radioligand binding in intact cells. No changes were observed on the effects of low-temperature after blocking receptor internalization in α(2C)-AR transfected HEK293T cells. In contrast, two pharmacological chaperones, dimethyl sulfoxide and glycerol, increased the cell surface receptor levels at 37°C, but not at 30°C. Further, at 37°C α(2C)-AR is co-localized with endoplasmic reticulum markers, but not with the lysosomal markers. Treatment with three distinct HSP90 inhibitors, radicicol, macbecin and 17-DMAG significantly enhanced α(2C)-AR cell surface levels at 37°C, but these inhibitors had no effect at 30°C. Similar results were obtained after decreasing the HSP90 cellular levels using specific siRNA. Co-immunoprecipitation experiments demonstrated that α(2C)-AR interacts with HSP90 and this interaction is decreased at 30°C. The contractile response to endogenous α(2C)-AR stimulation in rat tail artery was also enhanced at reduced temperature. Similar to HEK293T cells, HSP90 inhibition increased the α(2C)-AR contractile effects only at 37°C. Moreover, exposure to low-temperature of vascular smooth muscle cells from rat tail artery decreased the cellular levels of HSP90, but did not change HSP70 levels. These data demonstrate that exposure to low-temperature augments the α(2C)-AR transport to the plasma membrane by releasing the inhibitory activity of HSP90 on the receptor traffic, findings which may have clinical relevance for the diagnostic and treatment of Raynaud Phenomenon.
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Registered trials
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