ATP synthase F1 complex catalytic subunit beta, mitochondrial (ATP5F1B)

ATP synthase F1 complex catalytic subunit beta, mitochondrial (ATP5F1B), is the β subunit of the catalytic F1 domain of mitochondrial ATP synthase (F1Fo ATPase)[1][6]. This enzyme complex is crucial for ATP synthesis during oxidative phosphorylation in the mitochondrial matrix, using the proton motive force generated by the electron transport chain to catalyze the formation of ATP from ADP and inorganic phosphate[1][4][5]. The F1 portion is composed of three α and three β subunits arranged alternately, with the β subunits carrying the primary catalytic sites[1][4][5]. Mutations in ATP5F1B or subunit malfunction have been linked to mitochondrial diseases, neurodegenerative disorders, and can be observed as secondary changes in metabolic and degenerative diseases[1][6]. ATP5F1B is essential for cell survival; its pharmacological inhibition is not therapeutically viable systemically due to its fundamental role in cellular energetics, but selective inhibition (e.g., by oligomycin) is a classical biochemical tool[1][6][7]. ATP synthase subunits, including the β subunit, are subject to regulatory phosphorylation, and dysfunction can cause altered ATP production, contributing to energetically demanding tissues' pathology such as brain and heart[2].

Other names

ATP5BATPMBATPSBEpididymis secretory protein Li 271HUMOP2Mitochondrial ATP synthase beta subunitMitochondrial ATP synthetase, beta subunitATP synthase subunit beta, mitochondrialATP synthase beta chainF1-ATPase beta subunitHEL-S-271

Direct enzyme inhibition (block of proton channel suppresses ATP synthesis/hydrolysis)[1][7] Allosteric modulation via phosphorylation or small molecule binding[2]