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Special Issue "Ion Channels as Marine Drug Targets 2021"

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: 15 December 2021.

Special Issue Editor

Special Issue Information

Dear Colleagues,

Animal venoms, especially of marine origin, are rich natural sources of bioactive compounds. The molecular targets of the latter are mainly ion (i.e., sodium, potassium, calcium, and chloride) channels with their numerous variants/subtypes. These venom molecules are exhibiting diverse potencies and selectivities and may have some therapeutic potential based on their cellular targets. Over the past decade, marine molecules have been widely studied, as they represent potential drugs to treat a variety of (human) pathologies, from pain to autoimmune and neurological diseases. As with the first edition that closed in 2020 (https://www.mdpi.com/journal/marinedrugs/special_issues/ion_channels_targets), this new Special Issue "Ion Channels as Marine Drug Targets 2021" of Marine Drugs is devoted to different aspects of marine (or marine-derived) molecules, from the discovery and structural characterization to the pharmacology and molecular engineering to develop "novel" candidate chemotherapeutic drugs targeting the ion channel(s).

Dr. Jean-Marc Sabatier
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 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. Marine Drugs 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 2400 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

  • ion channel
  • immunomodulator
  • pain killer
  • candidate drug
  • marine drug
  • structure-activity relationships
  • venomous marine animal
  • animal venom
  • toxin
  • sea snake
  • sea anemone
  • jellyfish
  • stingray
  • puffer fish
  • scorpion fish
  • marine cone snail

Related Special Issue

Published Papers (2 papers)

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Research

Article
Brevetoxin and Conotoxin Interactions with Single-Domain Voltage-Gated Sodium Channels from a Diatom and Coccolithophore
Mar. Drugs 2021, 19(3), 140; https://doi.org/10.3390/md19030140 - 02 Mar 2021
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Abstract
The recently characterized single-domain voltage-gated ion channels from eukaryotic protists (EukCats) provide an array of novel channel proteins upon which to test the pharmacology of both clinically and environmentally relevant marine toxins. Here, we examined the effects of the hydrophilic µ-CTx PIIIA and [...] Read more.
The recently characterized single-domain voltage-gated ion channels from eukaryotic protists (EukCats) provide an array of novel channel proteins upon which to test the pharmacology of both clinically and environmentally relevant marine toxins. Here, we examined the effects of the hydrophilic µ-CTx PIIIA and the lipophilic brevetoxins PbTx-2 and PbTx-3 on heterologously expressed EukCat ion channels from a marine diatom and coccolithophore. Surprisingly, none of the toxins inhibited the peak currents evoked by the two EukCats tested. The lack of homology in the outer pore elements of the channel may disrupt the binding of µ-CTx PIIIA, while major structural differences between mammalian sodium channels and the C-terminal domains of the EukCats may diminish interactions with the brevetoxins. However, all three toxins produced significant negative shifts in the voltage dependence of activation and steady state inactivation, suggesting alternative and state-dependent binding conformations that potentially lead to changes in the excitability of the phytoplankton themselves. Full article
(This article belongs to the Special Issue Ion Channels as Marine Drug Targets 2021)
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Article
α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells
Mar. Drugs 2021, 19(2), 118; https://doi.org/10.3390/md19020118 - 21 Feb 2021
Viewed by 647
Abstract
Among the brain tumors, glioma is the most common. In general, different biochemical mechanisms, involving nicotinic acetylcholine receptors (nAChRs) and the arachidonic acid cascade are involved in oncogenesis. Although the engagement of the latter in survival and proliferation of rat C6 glioma has [...] Read more.
Among the brain tumors, glioma is the most common. In general, different biochemical mechanisms, involving nicotinic acetylcholine receptors (nAChRs) and the arachidonic acid cascade are involved in oncogenesis. Although the engagement of the latter in survival and proliferation of rat C6 glioma has been shown, there are practically no data about the presence and the role of nAChRs in C6 cells. In this work we studied the effects of nAChR antagonists, marine snail α-conotoxins and snake α-cobratoxin, on the survival and proliferation of C6 glioma cells. The effects of the lipoxygenase and cyclooxygenase inhibitors either alone or together with α-conotoxins and α-cobratoxin were studied in parallel. It was found that α-conotoxins and α-cobratoxin promoted the proliferation of C6 glioma cells, while nicotine had practically no effect at concentrations below 1 µL/mL. Nordihydroguaiaretic acid, a nonspecific lipoxygenase inhibitor, and baicalein, a 12-lipoxygenase inhibitor, exerted antiproliferative and cytotoxic effects on C6 cells. nAChR inhibitors weaken this effect after 24 h cultivation but produced no effects at longer times. Quantitative real-time polymerase chain reaction showed that mRNA for α4, α7, β2 and β4 subunits of nAChR were expressed in C6 glioma cells. This is the first indication for involvement of nAChRs in mechanisms of glioma cell proliferation. Full article
(This article belongs to the Special Issue Ion Channels as Marine Drug Targets 2021)
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