ArticleStem cell research & therapy2016
Mitochondrial co-chaperone protein Tid1 is required for energy homeostasis during skeletal myogenesis.
Article in Stem cell research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 20 citations in OpenAlex.
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Regimen on Dnaja3 haploinsufficiency mediated sarcopenic obesity with imbalanced mitochondrial homeostasis and lipid metabolism.Journal of cachexia, sarcopenia and muscle · 2024Article
- Characterization of PANoptosis-related genes and the immune landscape in moyamoya disease.Scientific reports · 2024Article
- Putting human Tid-1 in context: an insight into its role in the cell and in different disease states.Cell communication and signaling : CCS · 2022Review
- Characterisation of the heat shock protein Tid and its involvement in stress response regulation inFrontiers in physiology · 2022Article
- Regulation of p53 and Cancer Signaling by Heat Shock Protein 40/J-Domain Protein Family Members.International journal of molecular sciences · 2021Review
- Mitochondrial HSP70 Chaperone System-The Influence of Post-Translational Modifications and Involvement in Human Diseases.International journal of molecular sciences · 2021Review
- Article
- DNAJA3/Tid1 Is Required for Mitochondrial DNA Maintenance and Regulates Migration and Invasion of Human Gastric Cancer Cells.Cancers · 2020Article
- Article
- Redox Aspects of Chaperones in Cardiac Function.Frontiers in physiology · 2018Review
- HSP40 co-chaperone protein Tid1 suppresses metastasis of head and neck cancer by inhibiting Galectin-7-TCF3-MMP9 axis signaling.Theranostics · 2018Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTid1 is a mitochondrial co-chaperone protein and its transcript is abundantly expressed in skeletal muscle tissues. However, the physiological function of Tid1 during skeletal myogenesis remains unclear.
methodsIn vitro induced differentiation assay of mouse myoblast C2C12 cells was applied to examine the physiological role of Tid1 during skeletal myogenesis. In addition, transgenic mice with muscle specific (HSA-Cre) Tid1 deletion were established and examined to determine the physiological function of Tid1 during skeletal muscle development in vivo.
resultsExpression of Tid1 protein was upregulated in the differentiated C2C12 cells, and the HSA-Tid1
conclusionTogether, our results suggest that Tid1 deficiency reduces ATP production and abolishes mitochondrial activity, resulting in energy imbalance and promoting apoptosis of muscle cells during myogenesis. It will be of importance to understand the function of Tid1 during human muscular dystrophy in the future.
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