Atp5mc1, also known as ATP5G1, is one of the three proteins that comprise subunit c of the F0 complex of the mitochondrial ATP synthase. This gene is involved in the process of oxidative phosphorylation, which is crucial for generating ATP, the energy currency of cells [2].

In terms of disease associations, Atp5mc1 has been linked to several conditions. In sepsis, its gene expression level showed a negative correlation with sepsis risk, suggesting a potential protective role [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 pathogenesis of schizophrenia [3]. In striped hamsters, down-regulation of Atp5mc1 was noted during flea parasitism, highlighting its role in mitochondrial function during oxidative stress [4]. In sheep, the gene was downregulated in the hypothalamus of those fed nutrient-deficient diets, potentially related to voluntary feed intake regulation [5]. In radioresistant triple-negative breast cancer cells, co-treatment with certain compounds 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 through its role in the F0 complex of mitochondrial ATP synthase. Research across various models has revealed its associations with multiple disease conditions, including sepsis, schizophrenia, and responses to parasitism, nutrient deficiency, and cancer treatment. These findings emphasize the importance of studying Atp5mc1 to understand disease mechanisms and potentially develop new therapeutic strategies.