Atp5mc1-KO Mouse

Atp5mc1, also known as ATP5G1, is one of the three proteins that comprise subunit c of the F0 complex of the mitochondrial ATP synthase. It is involved in the oxidative phosphorylation pathway, which is crucial for ATP synthesis in mitochondria, and thus plays a significant role in cellular energy metabolism [2].

In various studies, Atp5mc1 has been associated with different disease conditions. In sepsis, its gene expression level showed a negative correlation with the risk of sepsis, suggesting its potential role in the pathogenesis of this condition [1]. In schizophrenia patients, significantly decreased Atp5mc1 mRNA expression levels were observed in plasma and peripheral blood mononuclear cells, indicating its possible involvement in the disease mechanism [3]. In striped hamsters parasitized by fleas, down-regulation of Atp5mc1 was noted, highlighting the importance of mitochondrial function in oxidative stress during host-ectoparasite interactions [4]. In young sheep fed nutrient-deficient diets, Atp5mc1 was downregulated in the hypothalamus, which might be related to the regulation of voluntary feed intake [5]. In radioresistant triple-negative breast cancer cells, co-treatment with melatonin and ortho-topolin riboside decreased Atp5mc1 expression, inhibiting mitochondrial respiration and cell proliferation [6]. In GFM1 knockout cells, upregulation of Atp5mc1 was seen as a compensatory mechanism in response to impaired mitochondrial function [7].

In conclusion, Atp5mc1 is essential for mitochondrial ATP synthesis and cellular energy metabolism. Its abnormal expression is associated with multiple disease states such as sepsis, schizophrenia, host-ectoparasite interactions, feed intake regulation, breast cancer, and mitochondrial function impairment. Research on Atp5mc1 helps to better understand the underlying mechanisms of these diseases and may provide potential therapeutic targets.