G-Protein-Coupled Receptors (GPCRs)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 4943

Special Issue Editor


E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, The University of British Columbiadisabled, Vancouver, BC, Canada
Interests: cancer biology; neurogenerative diseases; aging; BBB; diabetes; peptide processing; G-protein coupled receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

G-protein-coupled receptors (GPCRs) are the cell surface protein that constitute the largest family in the human genome (>800gene), and are involved in a wide variety of function in the peripheral and central system. GPCRs, primarily confined within the plasma membrane, and their structural findings revealed that they consist of seven transmembrane-spanning α-helix domains linked by three altering intracellular and extracellular loops and N- and C-terminals. GPCRs have the ability to bind or are activated by multiple ligands, including hormones, photons, ions, neurotransmitters, odorants, peptides, and light, and are involved in the regulation of multiple signaling pathways. The majority of transduction events in cells are under the influence of GPCRs, which is a testament to their significance as a major target of therapeutic drug discovery; at present, >40% of therapeutic drugs represent GPCR, worth an estimated >$850 billion. In the last two decades, our understanding regarding GPCRs’ functionality and pharmacology has significantly changed. The concept that GPCRs exist and function in a monomeric entity has been rephrased, and growing pharmacological, biochemical, and biophysical evidence supports that GPCRs form functionally active homo- and hetero-dimers, even a higher order of oligomers, and modulate pharmacological properties and receptor mediated regulation of downstream signaling pathways that are different from the native receptor. Despite recent progress in the field of GPCRs, the structure biology of these surface proteins is poorly understood; however, functional interactions between different GPCRs, including adrenergic, cannabinoid, GABA, dopamine, opioid, and somatostatin receptor subtypes are now well established.

As Guest Editor, I invite submission of manuscripts dealing with different aspects of GPCRs for publication in this Special Issue of Biomedicine.

Prof. Ujendra Kumar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • agonist
  • dimerization
  • G-proteins
  • receptor coupling
  • G-protein-coupled receptor kinases
  • G-protein-coupled receptors
  • internalization
  • ligand binding
  • monomers
  • pharmacology phosphorylation
  • signaling pathways

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

19 pages, 2154 KiB  
Article
UV-B Filter Octylmethoxycinnamate Is a Modulator of the Serotonin and Histamine Receptors in Human Umbilical Arteries
by Margarida Lorigo, Carla Quintaneiro, Luiza Breitenfeld and Elisa Cairrao
Biomedicines 2022, 10(5), 1054; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10051054 - 03 May 2022
Cited by 2 | Viewed by 1705
Abstract
Every day, people use personal care products containing UV filters. Although their use initially showed a protective role, toxicity is a concern for human health as several UV filters are endocrine-disrupting chemicals (EDCs). Exposure to EDCs may induce cardiovascular diseases and can affect [...] Read more.
Every day, people use personal care products containing UV filters. Although their use initially showed a protective role, toxicity is a concern for human health as several UV filters are endocrine-disrupting chemicals (EDCs). Exposure to EDCs may induce cardiovascular diseases and can affect the health of sensitive people, such as pregnant women. Currently, the world’s most widely used UV-B filter is octylmethoxycinnamate (OMC), an EDC. However, the disruptive effects on pregnant women are little known. The present work proposed to understand how long-term exposure to OMC affects vascular homeostasis. Endothelium-denuded human umbilical artery (HUA) rings were incubated in an organ bath system. Long-term effects of exposure to OMC (0.001–50 μmol/L) were evaluated on the contractile responses of HUA to the application of the contractile agents, serotonin (5-HT) and histamine (Hist). To investigate in more detail the vascular mode of action of OMC, through which it impairs the vascular homeostasis of HUA, the activity and expression of different 5-HT and Hist-receptors involved in contractility processes were studied. Our findings pointed out an increase in the reactivity of HUA to 5-HT and Hist due to OMC exposure. These alterations in reactivity may be precursors of preeclampsia development and/or gestational hypertension. Full article
(This article belongs to the Special Issue G-Protein-Coupled Receptors (GPCRs))
Show Figures

Graphical abstract

20 pages, 4419 KiB  
Article
RGS4-Deficiency Alters Intracellular Calcium and PKA-Mediated Control of Insulin Secretion in Glucose-Stimulated Beta Islets
by Guillaume Bastin, Lemieux Luu, Battsetseg Batchuluun, Alexandra Mighiu, Stephanie Beadman, Hangjung Zhang, Changhao He, Dana Al Rijjal, Michael B. Wheeler and Scott P. Heximer
Biomedicines 2021, 9(8), 1008; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9081008 - 13 Aug 2021
Cited by 6 | Viewed by 2461
Abstract
A number of diverse G-protein signaling pathways have been shown to regulate insulin secretion from pancreatic β-cells. Accordingly, regulator of G-protein signaling (RGS) proteins have also been implicated in coordinating this process. One such protein, RGS4, is reported to show both positive and [...] Read more.
A number of diverse G-protein signaling pathways have been shown to regulate insulin secretion from pancreatic β-cells. Accordingly, regulator of G-protein signaling (RGS) proteins have also been implicated in coordinating this process. One such protein, RGS4, is reported to show both positive and negative effects on insulin secretion from β-cells depending on the physiologic context under which it was studied. We here use an RGS4-deficient mouse model to characterize previously unknown G-protein signaling pathways that are regulated by RGS4 during glucose-stimulated insulin secretion from the pancreatic islets. Our data show that loss of RGS4 results in a marked deficiency in glucose-stimulated insulin secretion during both phase I and phase II of insulin release in intact mice and isolated islets. These deficiencies are associated with lower cAMP/PKA activity and a loss of normal calcium surge (phase I) and oscillatory (phase II) kinetics behavior in the RGS4-deficient β-cells, suggesting RGS4 may be important for regulation of both Gαi and Gαq signaling control during glucose-stimulated insulin secretion. Together, these studies add to the known list of G-protein coupled signaling events that are controlled by RGS4 during glucose-stimulated insulin secretion and highlight the importance of maintaining normal levels of RGS4 function in healthy pancreatic tissues. Full article
(This article belongs to the Special Issue G-Protein-Coupled Receptors (GPCRs))
Show Figures

Graphical abstract

Back to TopTop