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Biomolecules
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Advances in Cellular Biophysics: Transport and Mechanics
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Advances in Cellular Biophysics: Transport and Mechanics

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

Deadline for manuscript submissions: 30 April 2025 | Viewed by 3522

Special Issue Editors

Prof. Dr. Boris Musset

E-Mail Website
Guest Editor
Center of Physiology, Pathophysiology and Biophysics, Paracelsus Medical University, 90419 Nuremberg, Germany
Interests: ion transport; respiratory burst; proton transport; structure function relationship; electron transport
Prof. Dr. Peter Pohl

E-Mail Website
Guest Editor
Institute of Biophysics, Johannes Kepler University Linz, Gruberstraße 40, 4020 Linz, Austria
Interests: membrane transport; interfacial protons; water channels; protein–membrane translocation; membrane domains
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to a Special Issue focusing on the topic of “Cellular Biophysics: Transport and Mechanics”. Here, we would like to document the proceedings of the Cellular Biophysics (Section III) International Workshop of the German Biophysical Society (DGfB). Moreover, the interdisciplinary character of the workshop features results from many distinct branches of research, such as physics, biochemistry, physiology, medicine, molecular biology, pharmacology, and biology. Clustering these branches of research grants a unique opportunity to exchange knowledge and scientific progress, as well as state-of-the-art techniques. Substantial insights into the rapidly developing topic of cellular biophysics shall be presented, converging on the topic of membrane transport.

Membrane transport is an essential part of cell function and communication. Therefore, membrane transport impacts almost all pathologies known today, from neuronal, immunological, cardiovascular, metabolic disorders to even cancer. Deciphering the complex and unidentified mechanisms of membrane transport ultimately may lead to comprehension, control, drug development, and finally medical treatment or technological inventions that further improve the quality of life.

We look forward to receiving your contributions.

Prof. Dr. Boris Musset
Prof. Dr. Peter Pohl
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 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. Biomolecules 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 2700 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

  • membrane transport
  • ion transport
  • cellular biophysics
  • applied science
  • basic science

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Published Papers (3 papers)

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Research

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31 pages, 4414 KiB  
Article
Biophysical Properties of Somatic Cancer Mutations in the S4 Transmembrane Segment of the Human Voltage-Gated Proton Channel hHV1
by Christophe Jardin, Christian Derst, Arne Franzen, Iryna Mahorivska, Thomas E. DeCoursey, Boris Musset and Gustavo Chaves
Biomolecules 2025, 15(2), 156; https://doi.org/10.3390/biom15020156 - 21 Jan 2025
Viewed by 684
Abstract
Somatic mutations are common in cancer, with only a few driving the progression of the disease, while most are silent passengers. Some mutations may hinder or even reverse cancer progression. The voltage-gated proton channel (HV1) plays a key role in cellular [...] Read more.
Somatic mutations are common in cancer, with only a few driving the progression of the disease, while most are silent passengers. Some mutations may hinder or even reverse cancer progression. The voltage-gated proton channel (HV1) plays a key role in cellular pH homeostasis and shows increased expression in several malignancies. Inhibiting HV1 in cancer cells reduces invasion, migration, proton extrusion, and pH recovery, impacting tumor progression. Focusing on HVCN1, the gene coding for the human voltage-gated proton channel (hHV1), 197 mutations were identified from three databases: 134 missense mutations, 51 sense mutations, and 12 introducing stop codons. These mutations cluster in two hotspots: the central region of the N-terminus and the region coding for the S4 transmembrane domain, which contains the channel’s voltage sensor. Five somatic mutations within the S4 segment (R205W, R208W, R208Q, G215E, and G215R) were selected for electrophysiological analysis and MD simulations. The findings reveal that while all mutants remain proton-selective, they all exhibit reduced effective charge displacement and proton conduction. The mutations differentially affect hHV1 kinetics, with the most pronounced effects observed in the two Arg-to-Trp substitutions. Mutation of the first voltage-sensing arginine (R1) to tryptophan (R205W) causes proton leakage in the closed state, accelerates channel activation, and diminishes the voltage dependence of gating. Except for R205W, the mutations promote the deactivated channel configuration. Altogether, these data are consistent with impairment of hHV1 function by mutations in the S4 transmembrane segment, potentially affecting pH homeostasis of tumor cells. Full article
(This article belongs to the Special Issue Advances in Cellular Biophysics: Transport and Mechanics)
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Review

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13 pages, 918 KiB  
Review
Charge Movements and Conformational Changes: Biophysical Properties and Physiology of Voltage-Dependent GPCRs
by Andreas Rinne and Moritz Bünemann
Biomolecules 2024, 14(12), 1652; https://doi.org/10.3390/biom14121652 - 23 Dec 2024
Viewed by 841
Abstract
G protein-coupled receptors (GPCRs) regulate multiple cellular functions and represent important drug targets. More than 20 years ago, it was noted that GPCR activation (agonist binding) and signaling (G protein activation) are dependent on the membrane potential (VM). While it is [...] Read more.
G protein-coupled receptors (GPCRs) regulate multiple cellular functions and represent important drug targets. More than 20 years ago, it was noted that GPCR activation (agonist binding) and signaling (G protein activation) are dependent on the membrane potential (VM). While it is now proven that many GPCRs display an intrinsic voltage dependence, the molecular mechanisms of how GPCRs sense depolarization of the plasma membrane are less well defined. This review summarizes the current knowledge of voltage-dependent signaling in GPCRs. We describe how voltage dependence was discovered in muscarinic receptors, present an overview of GPCRs that are regulated by voltage, and show how biophysical properties of GPCRs led to the discovery of voltage-sensing mechanisms in those receptors. Furthermore, we summarize physiological functions that have been shown to be regulated by voltage-dependent GPCR signaling of endogenous receptors in excitable tissues, such as the nervous system or the heart. Finally, we discuss challenges that remain in analyzing voltage-dependent signaling of GPCRs in vivo and present an outlook on experimental applications of the interesting concept of GPCR signaling. Full article
(This article belongs to the Special Issue Advances in Cellular Biophysics: Transport and Mechanics)
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19 pages, 1700 KiB  
Review
Ca2+ Signaling in Cardiovascular Fibroblasts
by Andreas Rinne and Florentina Pluteanu
Biomolecules 2024, 14(11), 1365; https://doi.org/10.3390/biom14111365 - 27 Oct 2024
Viewed by 1275
Abstract
Fibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such as collagen, to form a [...] Read more.
Fibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such as collagen, to form a scar. Once the healing process is terminated, most myofibroblasts undergo apoptosis. However, in some tissues, such as the heart, myofibroblasts remain active and sensitive to neurohumoral factors and inflammatory mediators, which lead eventually to excessive organ fibrosis. Many cellular processes involved in fibroblast activation, including cell proliferation, protein secretion and cell contraction, are highly regulated by intracellular Ca2+ signals. This review summarizes current research on Ca2+ signaling pathways underlying fibroblast activation. We present receptor- and ion channel-mediated Ca2+ signaling pathways, discuss how localized Ca2+ signals of the cell nucleus may be involved in fibroblast activation and present Ca2+-sensitive transcription pathways relevant for fibroblast biology. When investigated, we highlight how the function of Ca2+-handling proteins changes during cardiac and pulmonary fibrosis. Many aspects of Ca2+ signaling remain unexplored in different types of cardiovascular fibroblasts in relation to pathologies, and a better understanding of Ca2+ signaling in fibroblasts will help to design targeted therapies against fibrosis. Full article
(This article belongs to the Special Issue Advances in Cellular Biophysics: Transport and Mechanics)
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