Tubulin βII and βIII Isoforms as the Regulators of VDAC Channel Permeability in Health and Disease.
Marju PuurandKersti TeppNatalja TimohhinaJekaterina AidIgor ShevchukVladimir ChekulayevTuuli KaambrePublished in: Cells (2019)
In recent decades, there have been several models describing the relationships between the cytoskeleton and the bioenergetic function of the cell. The main player in these models is the voltage-dependent anion channel (VDAC), located in the mitochondrial outer membrane. Most metabolites including respiratory substrates, ADP, and Pi enter mitochondria only through VDAC. At the same time, high-energy phosphates are channeled out and directed to cellular energy transfer networks. Regulation of these energy fluxes is controlled by β-tubulin, bound to VDAC. It is also thought that β-tubulin‒VDAC interaction modulates cellular energy metabolism in cancer, e.g., switching from oxidative phosphorylation to glycolysis. In this review we focus on the described roles of unpolymerized αβ-tubulin heterodimers in regulating VDAC permeability for adenine nucleotides and cellular bioenergetics. We introduce the Mitochondrial Interactosome model and the function of the βII-tubulin subunit in this model in muscle cells and brain synaptosomes, and also consider the role of βIII-tubulin in cancer cells.
Keyphrases
- energy transfer
- oxidative stress
- healthcare
- public health
- induced apoptosis
- endothelial cells
- mental health
- cell death
- squamous cell carcinoma
- white matter
- skeletal muscle
- bone marrow
- cell cycle arrest
- cell proliferation
- risk assessment
- cell therapy
- multiple sclerosis
- social media
- young adults
- papillary thyroid
- reactive oxygen species
- blood brain barrier
- brain injury
- health information
- climate change
- respiratory tract
- childhood cancer