BAX and BAK are generally considered as fully interchangeable for mitochondrial permeabilization and consequent apoptotic cell death. Garcia-Saez and colleagues have recently documented striking kinetic differences that influence BAX and BAK oligomerization at the mitochondrial surface. These data have important implications for inflammatory responses driven by mitochondrial DNA.
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Funding
The LG lab is supported by a Breakthrough Level 2 grant from the US DoD BRCP (#BC180476P1), by the 2019 Laura Ziskin Prize in Translational Research (#ZP-6177, PI: Formenti) from the Stand Up to Cancer (SU2C), by a Mantle Cell Lymphoma Research Initiative (MCL-RI, PI: Chen-Kiang) grant from the Leukemia and Lymphoma Society (LLS), by a startup grant from the Dept. of Radiation Oncology at Weill Cornell Medicine (New York, US), by a Rapid Response Grant from the Functional Genomics Initiative (New York, US), by industrial collaborations with Lytix Biopharma (Oslo, Norway) and Phosplatin (New York, US), and by donations from Phosplatin (New York, US), the Luke Heller TECPR2 Foundation (Boston, US), Sotio a.s. (Prague, Czech Republic), Onxeo (Paris, France), Ricerchiamo (Brescia, Italy), and Noxopharm (Chatswood, Australia).
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TY and LG conceived the article, wrote the manuscript and prepared display items. LG addressed editorial requests.
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LG has been holding research contracts with Lytix Biopharma and Phosplatin, and has received consulting/advisory honoraria from Boehringer Ingelheim, AstraZeneca, OmniSEQ, Onxeo, The Longevity Labs, Inzen, Phosplatin, and the Luke Heller TECPR2 Foundation. All other authors have no conflicts to declare.
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Yamazaki, T., Galluzzi, L. BAX and BAK dynamics control mitochondrial DNA release during apoptosis. Cell Death Differ 29, 1296–1298 (2022). https://doi.org/10.1038/s41418-022-00985-2
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DOI: https://doi.org/10.1038/s41418-022-00985-2
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