Mitochondrial co-chaperone protein Tid1 is required for energy homeostasis during skeletal myogenesis.
Li-Hao ChengKai-Feng HungTe-Chang LeeChih-Yang HuangWen-Ting ChiuJeng-Fan LoTung-Fu HuangPublished in: Stem cell research & therapy (2016)
Together, 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.
Keyphrases
- oxidative stress
- muscular dystrophy
- cell cycle arrest
- induced apoptosis
- cell death
- endoplasmic reticulum stress
- endothelial cells
- pi k akt
- duchenne muscular dystrophy
- skeletal muscle
- induced pluripotent stem cells
- protein protein
- current status
- heat shock protein
- endoplasmic reticulum
- signaling pathway
- binding protein
- amino acid
- replacement therapy