ATP5B

ATP5B Full Name

ATP synthase, H+ transporting, mitochondrial F1 complex, beta polypeptide

ATP5B Introduction

ATP5B (ATP synthase, H+ transporting, mitochondrial F1 complex, beta polypeptide) encodes the beta subunit of the mitochondrial F1Fo-ATP synthase (Complex V), a key enzyme responsible for producing cellular ATP through oxidative phosphorylation. As one of the catalytic components of the F1 domain, ATP5B contains the nucleotide-binding site required for ATP synthesis and plays an essential role in converting the proton gradient generated by the mitochondrial electron transport chain into chemical energy. Because ATP5B directly controls mitochondrial energy output, alterations in its expression or function can disrupt cellular metabolism, increase oxidative stress, and impair tissues with high energy demands, making ATP5B an important target for studying mitochondrial dysfunction and metabolic disorders.

ATP5B is increasingly recognized as a critical regulator of cancer metabolism because tumor cells often undergo metabolic reprogramming to satisfy increased energy requirements for proliferation, invasion, and survival. Studies have demonstrated that ATP5B contributes to maintaining oxidative phosphorylation activity and supports tumor progression in several cancer types. For example, research on the TOMM34/ATP5B axis in liver cancer showed that ATP5B is required for TOMM34-mediated mitochondrial adaptation, ATP production, and metastatic behavior, while ATP5B suppression reduces cancer cell energy metabolism and migration. In addition, multi-omics analyses have identified ATP5B as a potential prognostic biomarker associated with tumor progression, including breast cancer, highlighting its value for investigating mitochondrial metabolic vulnerabilities and developing metabolism-targeted therapeutic strategies.

Beyond cancer, ATP5B is closely associated with mitochondrial genetic and metabolic diseases caused by impaired energy production. Mutations or abnormal regulation of ATP5B may compromise ATP synthase efficiency, leading to reduced oxidative phosphorylation capacity, altered reactive oxygen species (ROS) balance, and mitochondrial stress. Emerging studies investigating mitochondrial energy regulation have used ATP5B as a representative marker of ATP synthase activity, emphasizing its role in maintaining mitochondrial homeostasis and cellular bioenergetics. Due to its central position in mitochondrial ATP generation, ATP5B remains an important research target for understanding mitochondrial disorders, metabolic adaptation, neurodegenerative processes, and therapeutic approaches aimed at restoring cellular energy balance.

Alternate Names for ATP5B

ATP5B; ATP synthase, H+ transporting, mitochondrial F1 complex, beta polypeptide; ATPMB; ATPSB; HEL-S-271; ATP synthase subunit beta, mitochondrial; epididymis secretory protein Li 271; mitochondrial ATP synthase beta subunit; mitochondrial ATP synthetase, beta subunit;

• 1.Ősz F, et al.; Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels in C. elegans. Antioxidants (Basel). 2025, 14(1):76.
  2.Jin P, et al.; Disrupting metformin adaptation of liver cancer cells by targeting the TOMM34/ATP5B axis. EMBO Mol Med. 2022, 14(12):e16082.