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The Role of G Protein-Coupled Receptors (GPCRs) in Human Health...
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The Role of G Protein-Coupled Receptors (GPCRs) in Human Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 5335

Special Issue Editor

Dr. Ciria C. Hernandez

E-Mail Website
Guest Editor
Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
Interests: voltage and ligand gated ion channel structure and function; channelopathies; signaling transduction; G-protein coupled receptors structure and function; epilepsy and metabolism; variants and pathogenic mutations
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

G protein-coupled receptors (GPCRs) are a very large and diverse group of multimeric proteins that signal and modulate a wide variety of effectors within the cell. Each element (receptors, accessory proteins, kinases, endogenous ligands, ion channels) that specifically participates in the different signaling pathways is highly regulated within the amplification pathways of the responses mediated by the specific binding of ligands, whether they are agonists, antagonists, or allosteric modulators, to their specific GPCRs. The repertoire of responses is infinite, and each of these responses and points of modulation may be the initiation of defects in these signaling pathways and, therefore, the underlying pathophysiological substrate of the disease. In this Special Issue, we are particularly interested in new and innovative studies that bring together the most current perspectives on GPCR and defects related to GPCR function, leading to aberrant amplification of GPCR signaling, defects in internalization, endocytosis processes, and defects or impairment in ion channel coupling pathways and at any relevant physiological regulatory point in GPCR signaling.

Dr. Ciria C. Hernandez
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • GPCRs
  • ion channels
  • mutants
  • signaling
  • endocytosis
  • expression
  • internalization
  • kinases
  • endogenous ligands
  • arrestins
  • phosphorylation
  • glycosylation

Published Papers (3 papers)

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Research

18 pages, 3000 KiB  
Article
The CaSR Modulator NPS-2143 Reduced UV-Induced DNA Damage in Skh:hr1 Hairless Mice but Minimally Inhibited Skin Tumours
by Chen Yang, Mark Stephen Rybchyn, Warusavithana Gunawardena Manori De Silva, Jim Matthews, Katie Marie Dixon, Andrew J. A. Holland, Arthur David Conigrave and Rebecca Sara Mason
Int. J. Mol. Sci. 2023, 24(5), 4921; https://doi.org/10.3390/ijms24054921 - 03 Mar 2023
Viewed by 1490
Abstract
The calcium-sensing receptor (CaSR) is an important regulator of epidermal function. We previously reported that knockdown of the CaSR or treatment with its negative allosteric modulator, NPS-2143, significantly reduced UV-induced DNA damage, a key factor in skin cancer development. We subsequently wanted to [...] Read more.
The calcium-sensing receptor (CaSR) is an important regulator of epidermal function. We previously reported that knockdown of the CaSR or treatment with its negative allosteric modulator, NPS-2143, significantly reduced UV-induced DNA damage, a key factor in skin cancer development. We subsequently wanted to test whether topical NPS-2143 could also reduce UV-DNA damage, immune suppression, or skin tumour development in mice. In this study, topical application of NPS-2143 (228 or 2280 pmol/cm2) to Skh:hr1 female mice reduced UV-induced cyclobutane pyrimidine dimers (CPD) (p < 0.05) and oxidative DNA damage (8-OHdG) (p < 0.05) to a similar extent as the known photoprotective agent 1,25(OH)2 vitamin D3 (calcitriol, 1,25D). Topical NPS-2143 failed to rescue UV-induced immunosuppression in a contact hypersensitivity study. In a chronic UV photocarcinogenesis protocol, topical NPS-2143 reduced squamous cell carcinomas for only up to 24 weeks (p < 0.02) but had no other effect on skin tumour development. In human keratinocytes, 1,25D, which protected mice from UV-induced skin tumours, significantly reduced UV-upregulated p-CREB expression (p < 0.01), a potential early anti-tumour marker, while NPS-2143 had no effect. This result, together with the failure to reduce UV-induced immunosuppression, may explain why the reduction in UV-DNA damage in mice with NPS-2143 was not sufficient to inhibit skin tumour formation. Full article
(This article belongs to the Special Issue The Role of G Protein-Coupled Receptors (GPCRs) in Human Health and Diseases)
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18 pages, 2904 KiB  
Article
M3 Receptor Pathway Stimulates Rapid Transcription of the CB1 Receptor Activation through Calcium Signalling and the CNR1 Gene Promoter
by Pietro Marini, Philip Cowie, Ahmet Ayar, Guy S. Bewick, John Barrow, Roger G. Pertwee, Alasdair MacKenzie and Paolo Tucci
Int. J. Mol. Sci. 2023, 24(2), 1308; https://doi.org/10.3390/ijms24021308 - 09 Jan 2023
Viewed by 1718
Abstract
In this study, we have investigated a possible mechanism that enables CB1/M3 receptor cross-talk, using SH-SY5Y cells as a model system. Our results show that M3 receptor activation initiates signaling that rapidly upregulates the CNR1 gene, resulting in a [...] Read more.
In this study, we have investigated a possible mechanism that enables CB1/M3 receptor cross-talk, using SH-SY5Y cells as a model system. Our results show that M3 receptor activation initiates signaling that rapidly upregulates the CNR1 gene, resulting in a greatly potentiated CB1 receptor response to agonists. Calcium homeostasis plays an essential intermediary role in this functional CB1/M3 receptor cross-talk. We show that M3 receptor-triggered calcium release greatly increases CB1 receptor expression via both transcriptional and translational activity, by enhancing CNR1 promoter activity. The co-expression of M3 and CB1 receptors in brain areas such as the nucleus accumbens and amygdala support the hypothesis that the altered synaptic plasticity observed after exposure to cannabinoids involves cross-talk with the M3 receptor subtype. In this context, M3 receptors and their interaction with the cannabinoid system at the transcriptional level represent a potential pharmacogenomic target not only for the develop of new drugs for addressing addiction and tolerance. but also to understand the mechanisms underpinning response stratification to cannabinoids. Full article
(This article belongs to the Special Issue The Role of G Protein-Coupled Receptors (GPCRs) in Human Health and Diseases)
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12 pages, 2358 KiB  
Article
Berbamine Reduces Chloroquine-Induced Itch in Mice through Inhibition of MrgprX1
by Kunhi Ryu, Yunkyung Heo, Yechan Lee, Hyejin Jeon and Wan Namkung
Int. J. Mol. Sci. 2022, 23(22), 14321; https://doi.org/10.3390/ijms232214321 - 18 Nov 2022
Cited by 2 | Viewed by 1687
Abstract
Chloroquine (CQ) is an antimalaria drug that has been widely used for decades. However, CQ-induced pruritus remains one of the major obstacles in CQ treatment for uncomplicated malaria. Recent studies have revealed that MrgprX1 plays an essential role in CQ-induced itch. To date, [...] Read more.
Chloroquine (CQ) is an antimalaria drug that has been widely used for decades. However, CQ-induced pruritus remains one of the major obstacles in CQ treatment for uncomplicated malaria. Recent studies have revealed that MrgprX1 plays an essential role in CQ-induced itch. To date, a few MrgprX1 antagonists have been discovered, but they are clinically unavailable or lack selectivity. Here, a cell-based high-throughput screening was performed to identify novel antagonists of MrgprX1, and the screening of 2543 compounds revealed two novel MrgprX1 inhibitors, berbamine and closantel. Notably, berbamine potently inhibited CQ-mediated MrgprX1 activation (IC50 = 1.6 μM) but did not alter the activity of other pruritogenic GPCRs. In addition, berbamine suppressed the CQ-mediated phosphorylation of ERK1/2. Interestingly, CQ-induced pruritus was significantly reduced by berbamine in a dose-dependent manner, but berbamine had no effect on histamine-induced, protease-activated receptors 2-activating peptide-induced, and deoxycholic acid-induced itch in mice. These results suggest that berbamine is a novel, potent, and selective antagonist of MrgprX1 and may be a potential drug candidate for the development of therapeutic agents to treat CQ-induced pruritus. Full article
(This article belongs to the Special Issue The Role of G Protein-Coupled Receptors (GPCRs) in Human Health and Diseases)
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