Defects in the Transport Mechanism of Membrane Proteins and Related Diseases, 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 498

Special Issue Editor


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Guest Editor
Department of Medicine and Surgery, LUM University Giuseppe Degennaro Torre Rossi, 70010 Casamassima, Italy
Interests: structure/function relationship; transport mechanism; mitochondrial transport proteins; mitochondrial carrier diseases; mitochondrial carrier identification; design, synthesis and biological evaluation of new drugs against neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Following a very successful first run, we are pleased to announce the launch of the second edition of a Special Issue on ‘Defects in the Transport Mechanism of Membrane Proteins and Related Diseases’.

Membrane transport proteins play crucial roles across biological membranes and participate in cell physiology, metabolism and signaling, maintaining cellular homeostasis, and permitting the translocation of many classes of metabolites (i.e., sugar, amino acids, lipids, vitamins, inorganic ions and others). These proteins are essential for cellular functions ensuring cell survival in response to frequent stimuli of intracellular or environmental stress. Indeed, the transport mechanism exerted by membrane transport proteins, generating concentration gradients via active transport mechanisms, passive diffusion and ion channels, contributes to the regulation of biochemical pathways through correct cellular concentrations of substrates and products. Therefore, genetic mutations or the impairment of transport systems would turn out in defects in the transport mechanism with changes in the expression, activity and structure of proteins, which are manifested in different groups of neurodegenerative and metabolic diseases.

Hence, the purpose of this Special Issue “Defects in the Transport Mechanism of Membrane Proteins and Related Diseases" is to integrate current knowledge regarding physiological functions and the mechanisms of transport of a wide group of membrane transport proteins underlying their involvements in the initiation and progression of many diseases. Research papers and review manuscripts depicting a special focus on membrane transporters are invited for submission. Short communications will also be taken into consideration.

Dr. Daniela Valeria Miniero
Guest Editor

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Keywords

  • function, structure and folding of membrane transport proteins
  • pathological mutations
  • mechanism of transport
  • neurological and metabolic disease
  • transport of nanoparticles
  • organelle membranes
  • cellular function and signaling
  • bioenergetics
  • neuroinflammation
  • nanoformulations for drug targets

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Published Papers (1 paper)

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Review

23 pages, 2433 KiB  
Review
Massive Activation of GABAA Receptors: Rundown, Ionic and Neurodegenerative Consequences
by Sergey A. Menzikov, Danila M. Zaichenko, Aleksey A. Moskovtsev, Sergey G. Morozov and Aslan A. Kubatiev
Biomolecules 2025, 15(7), 1003; https://doi.org/10.3390/biom15071003 - 13 Jul 2025
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Abstract
The GABAA receptors, through a short-term interaction with a mediator, induce hyperpolarization of the membrane potential (Vm) via the passive influx of chloride ions (Cl) into neurons. The massive (or intense) activation of the GABAARs [...] Read more.
The GABAA receptors, through a short-term interaction with a mediator, induce hyperpolarization of the membrane potential (Vm) via the passive influx of chloride ions (Cl) into neurons. The massive (or intense) activation of the GABAARs by the agonist could potentially lead to depolarization/excitation of the Vm. Although the ionic mechanisms of GABAA-mediated depolarization remain incompletely understood, a combination of the outward chloride current and the inward bicarbonate current and the resulting pH shift are the main reasons for this event. The GABAA responses are determined by the ionic gradients—neuronal pH/bicarbonate homeostasis is maintained by carbonic anhydrase and electroneutral/electrogenic bicarbonate transporters and the chloride level is maintained by secondary active cation–chloride cotransporters. Massive activation can also induce the rundown effect of the receptor function. This rundown effect partly involves phosphorylation, Ca2+ and the processes of receptor desensitization. In addition, by various methods (including fluorescence and optical genetic methods), it has been shown that massive activation of GABAARs during pathophysiological activity is also associated with an increase in [Cl]i and a decline in the pH and ATP levels in neurons. Although the relationship between the neuronal changes induced by massive activation of GABAergic signaling and the risk of developing neurodegenerative disease has been extensively studied, the molecular determinants of this process remain somewhat mysterious. The aim of this review is to summarize the data on the relationship between the massive activation of inhibitory signaling and the ionic changes in neurons. The potential role of receptor dysfunction during massive activation and the resulting ionic and metabolic disruption in neurons during the manifestation of network/seizure activity will be considered. Full article
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