@article{oai:soar-ir.repo.nii.ac.jp:02000706, author = {Ikeda, Takahiro and Watanabe, Shun and Mitani, Takakazu}, issue = {2}, journal = {Bioscience, biotechnology, and biochemistry.}, month = {Feb}, note = {Genistein exerts antiadipogenic effects, but its target molecules remain unclear. Here, we delineated the molecular mechanism underlying the antiadipogenic effect of genistein. A pulldown assay using genistein-immobilized beads identified adenine nucleotide translocase-2 as a genistein-binding protein in adipocytes. Adenine nucleotide translocase-2 exchanges ADP/ATP through the mitochondrial inner membrane. Similar to the knockdown of adenine nucleotide translocase-2, genistein treatment decreased ADP uptake into the mitochondria and ATP synthesis. Genistein treatment and adenine nucleotide translocase-2 knockdown suppressed adipogenesis and increased phosphorylation of AMP-activated protein kinase. Adenine nucleotide translocase-2 knockdown reduced the transcriptional activity of CCAAT/enhancer-binding protein β, whereas AMP-activated protein kinase inhibition restored the suppression of adipogenesis by adenine nucleotide translocase-2 knockdown. These results indicate that genistein interacts directly with adenine nucleotide translocase-2 to suppress its function. The downregulation of adenine nucleotide translocase-2 reduces the transcriptional activity of CCAAT/enhancer-binding protein β via activation of AMP-activated protein kinase, which consequently represses adipogenesis., Article, Bioscience, biotechnology, and biochemistry. 86(2): 260-272 (2022)}, pages = {260--272}, title = {Genistein regulates adipogenesis by blocking the function of adenine nucleotide translocase-2 in the mitochondria}, volume = {86}, year = {2022} }