Article
Genetic suppression features ABHD18 as a Barth syndrome therapeutic target.
Nature - 1 Sept 2025
Masud Sanna N, Srivastava Anchal, Mero Patricia, Echezarreta Victoria Saba, Anderson Eve, van Buren Lennard, Wei Jiarun, Taylor David Thomson, Farias Adrian Granda, Mikolajewicz Nicholas, Shaw Angela, Murareanu Brandon M, Lohbihler Michelle, Carney Olivia Sniezek, van Heeringen Simon, Clijsters Linda, Sizova Olga, van Ameijde Jeroen, Nye Freya, Habsid Andrea, Nedyalkova Lucy, McDonald Laura, Simpson Craig, Wybenga-Groot Leanne, Brown Kevin R, Nho Nhi, Suciu Radu M, Chan Katherine, Tong Amy H Y, Vaz Frédéric M, Evers Bastiaan, Lesurf Robert, Papaz Tanya, Nutter Lauryl M J, Protze Stephanie, Billmann Maximilian, Costanzo Michael, Andrews Brenda J, Myers Chad L, Mital Seema, Vernon Hilary, Brummelkamp Thijn R, Boone Charles, Scott Ian C, Niphakis Micah J, Strathdee Douglas, Nijman Sebastian M B, Blomen Vincent A, Moffat Jason
Abstract excerpt
Cardiolipin (CL) is the signature phospholipid of the inner mitochondrial membrane, where it stabilizes electron transport chain protein complexes1. The final step in CL biosynthesis relates to its remodelling: the exchange of nascent acyl chains with longer, unsaturated chains1. However, the enzyme responsible for cleaving nascent CL (nCL) has remained elusive. Here, we describe ABHD18 as a candidate deacylase...
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