Mitochondrial porins, also known as voltage-dependent anion selective channels (VDACs), are pore-forming molecules of the outer mitochondrial membranes, involved in the regulation of metabolic flux between cytosol and mitochondria. Playing such an essential role, VDAC proteins are evolutionary conserved and isoforms are present in numerous species. The quest for specific function(s) related to the raise of multiple isoforms is an intriguing theme. The yeast genome is endowed with two different VDAC genes encoding for two distinct porin isoforms, definitely less characterized in comparison to mammalian counterpart. While yVDAC1 has been extensively studied, the second isoform, yVDAC2, is much less expressed, and has a still misunderstood function. This review will recapitulate the known and poorly known information in the literature, in the light of the growing interest about the features of VDAC isoforms in the cell.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8171188PMC
http://dx.doi.org/10.3389/fphys.2021.675708DOI Listing

Publication Analysis

Top Keywords

voltage-dependent anion
8
anion selective
8
isoforms
5
selective channel
4
channel isoforms
4
isoforms yeast
4
yeast expression
4
expression structure
4
structure functions
4
functions mitochondrial
4

Similar Publications

Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that is primarily known for causing severe joint and muscle symptoms, but its pathological effects have extended beyond these tissues. In this study, we conducted a comprehensive proteomic analysis across various organs in rodent and nonhuman primate models to investigate CHIKV's impact on organs beyond joints and muscles and to identify key host factors involved in its pathogenesis. Our findings reveal significant species-specific similarities and differences in immune responses and metabolic regulation, with proteins like Interferon-Stimulated Gene 15 (ISG15) and Retinoic Acid-Inducible Gene I (RIG-I) playing crucial roles in the anti-CHIKV defense.

View Article and Find Full Text PDF

Puerarin Protects Myocardium From Ischaemia/Reperfusion Injury by Inhibiting Ferroptosis Through Downregulation of VDAC1.

J Cell Mol Med

December 2024

Institute of Cardiovascular Surgical Diseases, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.

Despite improvements in interventional techniques leading to faster myocardial reperfusion postmyocardial infarction, there has been a significant rise in the occurrence of myocardial ischaemia/reperfusion injury (MI/RI). A deeper understanding of the underlying mechanisms of MI/RI could offer a crucial approach to reducing myocardial damage and enhancing patient outcomes. This study examined the myocardial protective properties of puerarin (PUE) in the context of MI/RI using hypoxia/reoxygenation (H/R) or ischaemia/reperfusion (I/R) injury models were employed in H9c2 cells and C57BL/6 mice.

View Article and Find Full Text PDF

Voltage-dependent anion channel (VDAC) is the primary conduit for regulated passage of ions and metabolites into and out of a mitochondrion. Calculating the solvation free energy for VDAC is crucial for understanding its stability, function, and interactions within the cellular environment. In this article, numerical schemes for computing the total solvation free energy for VDAC-comprising electrostatic, ideal gas, and excess free energies plus the nonpolar energy-are developed based on a nonuniform size modified Poisson-Boltzmann ion channel (nuSMPBIC) finite element solver along with tetrahedral meshes for VDAC proteins.

View Article and Find Full Text PDF

Labeling and isolating cell specific neuronal mitochondria and their functional analysis in mice post stroke.

Exp Neurol

December 2024

Department of Neurology, Henry Ford Health System, Detroit, MI 48202, United States of America. Electronic address:

Dendritic and axonal plasticity, which mediates neurobiological recovery after a stroke, critically depends on the mitochondrial function of neurons. To investigate, in vivo, neuronal mitochondrial function at the stroke recovery stage, we employed Mito-tag mice combined with cerebral cortical infection of AAV9 produced from plasmids carrying Cre-recombinase controlled by two neuronal promoters, synapsin-I (SYN1) and calmodulin-kinase IIa to induce expression of a hemagglutinin (HA)-tagged enhanced green fluorescence protein (EGFP) that localizes to mitochondrial outer membranes of SYN1 positive (SYN) and CaMKIIa positive (CaMKIIa) neurons. These mice were then subjected to permanent middle cerebral artery occlusion (MCAO) and sacrificed 14 days post stroke.

View Article and Find Full Text PDF

Identification of VDAC1 as a cardioprotective target of Ginkgolide B.

Chem Biol Interact

December 2024

School of Bioengineering, Zhuhai Campus of Zunyi Medical University, Zhuhai, 519000, China. Electronic address:

Ginkgolide B (GB), a compound derived from Ginkgo biloba, exhibits significant cardioprotective properties, although its precise molecular target has yet to be identified. In this study, we synthesized a biotin-labeled GB probe (GB-biotin) to identify the molecular targets of GB. Our experiments demonstrated that treatment with GB or GB-biotin reduced mitochondrial injury, restored mitochondrial membrane potential, and decreased cell apoptosis in a concentration-dependent manner.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!