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(Meta)Genomic, Functional, Structural and Evolutionary Analysis of Transport Systems
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(Meta)Genomic, Functional, Structural and Evolutionary Analysis of Transport Systems

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: 15 May 2024 | Viewed by 4288

Special Issue Editors

Dr. Arturo Medrano-Soto

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Guest Editor
Department of Molecular Biology, School of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA
Interests: bioinformatics; transport biology; molecular evolution; genomics
Dr. Milton Saier

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Guest Editor
Department of Molecular Biology, School of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA
Interests: molecular biology; transport biology; bioinformatics; genomics
Dr. Gabriel Moreno-Hagelsieb

E-Mail Website
Guest Editor
Department of Biology, Wilfred Laurier University, Waterloo, ON 2NL 3C5, Canada
Interests: gene regulation; transport biology; functional/comparative genomics; evolution; bioinformatics

Special Issue Information

Dear Colleagues,

Molecular transport systems are essential for life. They move molecules in and out of cells as well as organelles, thus playing critical roles in organismal physiology, homeostasis, and cell–cell communication. Transport proteins include channels, secondary carriers, primary active transporters, group translocators, and transmembrane electron carriers that selectively allow the passage of substrates through membranes. Whether transport is active or passive (depending on the energy requirements of the process), when transporters malfunction there can be catastrophic consequences for a cell. Due to their relevance to human health, more than 50% of all FDA-approved drugs target integral membrane proteins. This Special Issue presents a collection of papers conveying the state of the art in transport biology. These papers describe research ranging from experimental to bioinformatic approaches, contributing toward expanding our functional, evolutionary, and mechanistic understanding of transport systems in all domains of life.

The scope of this Special Issue will cover (but is not limited to) the following areas:

  1. Gene mutation and regulatory mechanisms of transport systems.
  2. Bioinformatics approaches to the study of transport systems.
  3. Ecological impact of molecular transport systems.
  4. Genomic and metagenomic analyses of transport systems.
  5. Three-dimensional structural approaches to the study of transport systems.
  6. Evolutionary analyses of transport systems.

Dr. Arturo Medrano-Soto
Dr. Milton Saier
Dr. Gabriel Moreno-Hagelsieb
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. 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

  • molecular transport
  • transport mechanisms
  • evolution
  • families and superfamilies
  • genomics
  • metagenomics
  • 3D structural insights
  • bioinformatics

Published Papers (2 papers)

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20 pages, 9212 KiB  
Article
Studies with Human-Induced Pluripotent Stem Cells Reveal That CTNS Mutations Can Alter Renal Proximal Tubule Differentiation
by Ramkumar Thiyagarajan and Mary Taub
Int. J. Mol. Sci. 2023, 24(23), 17004; https://doi.org/10.3390/ijms242317004 - 30 Nov 2023
Viewed by 3377
Abstract
Cystinosis is an autosomal recessive disease resulting from mutations in ctns, which encodes for cystinosin, a proton-coupled cystine transporter that exports cystine from lysosomes. The major clinical form, infantile cystinosis, is associated with renal failure due to the malfunctioning of the renal [...] Read more.
Cystinosis is an autosomal recessive disease resulting from mutations in ctns, which encodes for cystinosin, a proton-coupled cystine transporter that exports cystine from lysosomes. The major clinical form, infantile cystinosis, is associated with renal failure due to the malfunctioning of the renal proximal tubule (RPT). To examine the hypothesis that the malfunctioning of the cystinotic RPT arises from defective differentiation, human-induced pluripotent stem cells (hiPSCs) were generated from human dermal fibroblasts from an individual with infantile cystinosis, as well as a normal individual. The results indicate that both the cystinotic and normal hiPSCs are pluripotent and can form embryoid bodies (EBs) with the three primordial germ layers. When the normal hiPSCs were subjected to a differentiation regime that induces RPT formation, organoids containing tubules with lumens emerged that expressed distinctive RPT proteins, including villin, the Na+/H+ Exchanger (NHE) isoform 3 (NHE3), and the NHE Regulatory Factor 1 (NHERF1). The formation of tubules with lumens was less pronounced in organoids derived from cystinotic hiPSCs, although the organoids expressed villin, NHE3, and NHERF1. These observations can be attributed to an impairment in differentiation and/or by other defects which cause cystinotic RPTs to have an increased propensity to undergo apoptosis or other types of programmed cell death. Full article
(This article belongs to the Special Issue (Meta)Genomic, Functional, Structural and Evolutionary Analysis of Transport Systems)
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13 pages, 1196 KiB  
Review
Exploring the Pathophysiology of ATP-Dependent Potassium Channels in Insulin Resistance
by Nidia Samara Rodríguez-Rivera and Diana Barrera-Oviedo
Int. J. Mol. Sci. 2024, 25(7), 4079; https://doi.org/10.3390/ijms25074079 - 06 Apr 2024
Viewed by 425
Abstract
Ionic channels are present in eucaryotic plasma and intracellular membranes. They coordinate and control several functions. Potassium channels belong to the most diverse family of ionic channels that includes ATP-dependent potassium (KATP) channels in the potassium rectifier channel subfamily. These channels were initially [...] Read more.
Ionic channels are present in eucaryotic plasma and intracellular membranes. They coordinate and control several functions. Potassium channels belong to the most diverse family of ionic channels that includes ATP-dependent potassium (KATP) channels in the potassium rectifier channel subfamily. These channels were initially described in heart muscle and then in other tissues such as pancreatic, skeletal muscle, brain, and vascular and non-vascular smooth muscle tissues. In pancreatic beta cells, KATP channels are primarily responsible for maintaining the membrane potential and for depolarization-mediated insulin release, and their decreased density and activity may be related to insulin resistance. KATP channels’ relationship with insulin resistance is beginning to be explored in extra-pancreatic beta tissues like the skeletal muscle, where KATP channels are involved in insulin-dependent glucose recapture and their activation may lead to insulin resistance. In adipose tissues, KATP channels containing Kir6.2 protein subunits could be related to the increase in free fatty acids and insulin resistance; therefore, pathological processes that promote prolonged adipocyte KATP channel inhibition might lead to obesity due to insulin resistance. In the central nervous system, KATP channel activation can regulate peripheric glycemia and lead to brain insulin resistance, an early peripheral alteration that can lead to the development of pathologies such as obesity and Type 2 Diabetes Mellitus (T2DM). In this review, we aim to discuss the characteristics of KATP channels, their relationship with clinical disorders, and their mechanisms and potential associations with peripheral and central insulin resistance. Full article
(This article belongs to the Special Issue (Meta)Genomic, Functional, Structural and Evolutionary Analysis of Transport Systems)
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