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Special Issue "Membrane Channels in Physiology and Pathology"

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: 31 July 2022.

Special Issue Editors

Prof. Dr. Antonio Ferrer-Montiel
E-Mail Website
Guest Editor
Prof. Dr. Antonio Felipe
E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Medicine, Institut de Biomedicina, Universitat de Barcelona. Avda. Diagonal 643. 08028 Barcelona, Spain
Interests: voltage-dependent potassium channels; functional complex; oligomeric association; traffic; lipid rafts; post-translational modifications
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Ion channels are integral membrane proteins that play essential physiological roles. These specialized membrane proteins are responsible for the ions fluxes across the plasma membrane of all mammalian cells. Channels form functional oligomeric complexes by association with ancillary proteins, contributing to the cellular homeostasis and maintenance of health. Numerous cellular events control and are controlled by channel gating and kinetics. Membrane channels, with different ion selectivity, regulate membrane potential and excitability, shape the action potential, and elicit muscle contraction, among other cellular processes. Due to their contribution to the pathophysiology of various human diseases, these proteins are targets of many drugs, from antiepileptics to analgesics. Therefore, ion channel dysfunction at the onset of several human ailments are known as channelopathies, which include autoimmune, metabolic, neural, and cardiovascular diseases. The responsible abnormal behavior can be triggered by an altered function, impaired cell biology, genetic alterations, or drug-acquired response, among other events.

This Special Issue will assemble a series of reviews and research articles updating the state of knowledge on membrane channels in health and diseases. These contributions will inform of new progresses in the field and provide new therapeutic approaches for ion-channel-related diseases. This Special Issue is the third and renovated edition of the first Special Issue, “Membrane Channels in Human Diseases” launched in 2018, which has been successful in terms of global visibility and acceptance.

Prof. Dr. Antonio Ferrer-Montiel
Prof. Dr. Antonio Felipe
Guest Editors

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 papers will be 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

  • ion channels
  • nerve transmission
  • cardiac action potential
  • non excitable cell physiology
  • cancer and apoptosis
  • structure
  • channelopathies
  • drug discovery
  • molecular physiology
  • molecular architecture
  • genetics
  • bacterial physiology and infection
  • virus infection
  • plants physiology
  • toxins

Published Papers (2 papers)

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Research

Article
The Expression and Localisation of G-Protein-Coupled Inwardly Rectifying Potassium (GIRK) Channels Is Differentially Altered in the Hippocampus of Two Mouse Models of Alzheimer’s Disease
Int. J. Mol. Sci. 2021, 22(20), 11106; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011106 - 14 Oct 2021
Viewed by 202
Abstract
G protein-gated inwardly rectifying K+ (GIRK) channels are the main targets controlling excitability and synaptic plasticity on hippocampal neurons. Consequently, dysfunction of GIRK-mediated signalling has been implicated in the pathophysiology of Alzheimer´s disease (AD). Here, we provide a quantitative description on the [...] Read more.
G protein-gated inwardly rectifying K+ (GIRK) channels are the main targets controlling excitability and synaptic plasticity on hippocampal neurons. Consequently, dysfunction of GIRK-mediated signalling has been implicated in the pathophysiology of Alzheimer´s disease (AD). Here, we provide a quantitative description on the expression and localisation patterns of GIRK2 in two transgenic mice models of AD (P301S and APP/PS1 mice), combining histoblots and immunoelectron microscopic approaches. The histoblot technique revealed differences in the expression of GIRK2 in the two transgenic mice models. The expression of GIRK2 was significantly reduced in the hippocampus of P301S mice in a laminar-specific manner at 10 months of age but was unaltered in APP/PS1 mice at 12 months compared to age-matched wild type mice. Ultrastructural approaches using the pre-embedding immunogold technique, demonstrated that the subcellular localisation of GIRK2 was significantly reduced along the neuronal surface of CA1 pyramidal cells, but increased in its frequency at cytoplasmic sites, in both P301S and APP/PS1 mice. We also found a decrease in plasma membrane GIRK2 channels in axon terminals contacting dendritic spines of CA1 pyramidal cells in P301S and APP/PS1 mice. These data demonstrate for the first time a redistribution of GIRK channels from the plasma membrane to intracellular sites in different compartments of CA1 pyramidal cells. Altogether, the pre- and post-synaptic reduction of GIRK2 channels suggest that GIRK-mediated alteration of the excitability in pyramidal cells could contribute to the cognitive dysfunctions as described in the two AD animal models. Full article
(This article belongs to the Special Issue Membrane Channels in Physiology and Pathology)
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Article
Anti-Inflammatory Effect of Licochalcone A via Regulation of ORAI1 and K+ Channels in T-Lymphocytes
Int. J. Mol. Sci. 2021, 22(19), 10847; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910847 - 07 Oct 2021
Viewed by 452
Abstract
Calcium signaling plays a vital role in the regulation of various cellular processes, including activation, proliferation, and differentiation of T-lymphocytes, which is mediated by ORAI1 and potassium (K+) channels. These channels have also been identified as highly attractive therapeutic targets for [...] Read more.
Calcium signaling plays a vital role in the regulation of various cellular processes, including activation, proliferation, and differentiation of T-lymphocytes, which is mediated by ORAI1 and potassium (K+) channels. These channels have also been identified as highly attractive therapeutic targets for immune-related diseases. Licochalcone A is a licorice-derived chalconoid known for its multifaceted beneficial effects in pharmacological treatments, including its anti-inflammatory, anti-asthmatic, antioxidant, antimicrobial, and antitumorigenic properties. However, its anti-inflammatory effects involving ion channels in lymphocytes remain unclear. Thus, the present study aimed to investigate whether licochalcone A inhibits ORAI1 and K+ channels in T-lymphocytes. Our results indicated that licochalcone A suppressed all three channels (ORAI1, Kv1.3, and KCa3.1) in a concentration-dependent matter, with IC50 values of 2.97 ± 1.217 µM, 0.83 ± 1.222 µM, and 11.21 ± 1.07 µM, respectively. Of note, licochalcone A exerted its suppressive effects on the IL-2 secretion and proliferation in CD3 and CD28 antibody-induced T-cells. These results indicate that the use of licochalcone A may provide an effective treatment strategy for inflammation-related immune diseases. Full article
(This article belongs to the Special Issue Membrane Channels in Physiology and Pathology)
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