ArticleAntioxidants & redox signaling2014
Fus1/Tusc2 is a novel regulator of mitochondrial calcium handling, Ca2+-coupled mitochondrial processes, and Ca2+-dependent NFAT and NF-κB pathways in CD4+ T cells.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- An Evolutionarily Conserved TUSC2-OSCP Interface Suggests a Mitochondrial CaJournal of molecular biology · 2026Article
- Sex-specific transcriptomic effects of low-dose inorganic arsenic exposure on bone marrow-derived macrophages.Toxicology · 2025Article
- Loss of Mitochondrial Tusc2/Fus1 Triggers a Brain Pro-Inflammatory Microenvironment and Early Spatial Memory Impairment.International journal of molecular sciences · 2024Article
- Immunohistochemical and molecular evaluation of TUSC2 expression in breast cancer.Molecular biology reports · 2024Article
- The role of N-myristoyltransferase 1 in tumour development.Annals of medicine · 2023Review
- Pharmacological Modulation of Energy and Metabolic Pathways Protects Hearing in the Fus1/Tusc2 Knockout Model of Mitochondrial Dysfunction and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Mitochondrial Fus1/Tusc2 and cellular Ca2Cancer gene therapy · 2022Review
- Mitochondria dysfunction in CD8+ T cells as an important contributing factor for cancer development and a potential target for cancer treatment: a review.Journal of experimental & clinical cancer research : CR · 2022Review
- NEDD4 degrades TUSC2 to promote glioblastoma progression.Cancer letters · 2022Article
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- Insights into the post-translational modification and its emerging role in shaping the tumor microenvironment.Signal transduction and targeted therapy · 2021Review
- Mitochondrial Tumor Suppressors-The Energetic Enemies of Tumor Progression.Cancer research · 2021Review
- Dynamic Control of Mitochondrial CaFrontiers in cell and developmental biology · 2021Article
- TRPM8 facilitates proliferation and immune evasion of esophageal cancer cells.Bioscience reports · 2019Article
- Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression.Antioxidants (Basel, Switzerland) · 2018Review
- Mitofusin-2 mediated mitochondrial CaWorld journal of gastroenterology · 2017Article
- Novel Role of the Mitochondrial Protein Fus1 in Protection from Premature Hearing Loss via Regulation of Oxidative Stress and Nutrient and Energy Sensing Pathways in the Inner Ear.Antioxidants & redox signaling · 2017Article
- Article
- Tumor suppressor candidate 2 (TUSC2, FUS-1) and human cancers.Discovery medicine · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsFus1 has been established as mitochondrial tumor suppressor, immunomodulator, and antioxidant protein, but molecular mechanism of these activities remained to be identified. Based on putative calcium-binding and myristoyl-binding domains that we identified in Fus1, we explored our hypothesis that Fus1 regulates mitochondrial calcium handling and calcium-coupled processes.
resultsFus1 loss resulted in reduced rate of mitochondrial calcium uptake in calcium-loaded epithelial cells, splenocytes, and activated CD4(+) T cells. The reduced rate of mitochondrial calcium uptake in Fus1-deficient cells correlated with cytosolic calcium increase and dysregulation of calcium-coupled mitochondrial parameters, such as reactive oxygen species production, ΔμH(+), mitochondrial permeability transition pore opening, and GSH content. Inhibition of calcium efflux via mitochondria, Na(+)/Ca(2+) exchanger significantly improved the mitochondrial calcium uptake in Fus1(-/-) cells. Ex vivo analysis of activated CD4(+) T cells showed Fus1-dependent changes in calcium-regulated processes, such as surface expression of CD4 and PD1/PD-L1, proliferation, and Th polarization. Fus1(-/-) T cells showed increased basal expression of calcium-dependent NF-κB and NFAT targets but were unable to fully activate these pathways after stimulation. INNOVATION: Our results establish Fus1 as one of the few identified regulators of mitochondrial calcium handling. Our data support the idea that alterations in mitochondrial calcium dynamics could lead to the disruption of metabolic coupling in mitochondria that, in turn, may result in multiple cellular and systemic abnormalities.
conclusionOur findings suggest that Fus1 achieves its protective role in inflammation, autoimmunity, and cancer via the regulation of mitochondrial calcium and calcium-coupled parameters.
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