Small molecules targeting selective PCK1 and PGC-1α lysine acetylation cause anti-diabetic action through increased lactate oxidation.

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Bibliographic Details
Title: Small molecules targeting selective PCK1 and PGC-1α lysine acetylation cause anti-diabetic action through increased lactate oxidation.
Authors: Mutlu B; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA., Sharabi K; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA; Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Jerusalem, Israel., Sohn JH; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA., Yuan B; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, 655 Huntington Avenue, Boston, MA 02115, USA., Latorre-Muro P; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA., Qin X; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA., Yook JS; Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA., Lin H; Department of Molecular Medicine, The Wertheim UF Scripps Institute for Biomedical Innovation and Technology, University of Florida, Jupiter, FL 33458, USA., Yu D; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA., Camporez JPG; Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520-8020, USA; Department of Cellular & Molecular Physiology, Yale School of Medicine, New Haven, CT 06520-8020, USA., Kajimura S; Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA; Howard Hughes Medical Institute, Chevy Chase, MD 020815, USA., Shulman GI; Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520-8020, USA; Department of Cellular & Molecular Physiology, Yale School of Medicine, New Haven, CT 06520-8020, USA; Howard Hughes Medical Institute, Chevy Chase, MD 020815, USA., Hui S; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, 655 Huntington Avenue, Boston, MA 02115, USA., Kamenecka TM; Department of Molecular Medicine, The Wertheim UF Scripps Institute for Biomedical Innovation and Technology, University of Florida, Jupiter, FL 33458, USA., Griffin PR; Department of Molecular Medicine, The Wertheim UF Scripps Institute for Biomedical Innovation and Technology, University of Florida, Jupiter, FL 33458, USA., Puigserver P; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA. Electronic address: pere_puigserver@dfci.harvard.edu.
Source: Cell chemical biology [Cell Chem Biol] 2024 Oct 17; Vol. 31 (10), pp. 1772-1786.e5. Date of Electronic Publication: 2024 Sep 27.
Publication Type: Journal Article
Journal Info: Publisher: Cell Press Country of Publication: United States NLM ID: 101676030 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2451-9448 (Electronic) Linking ISSN: 24519448 NLM ISO Abbreviation: Cell Chem Biol Subsets: MEDLINE
Database: MEDLINE Ultimate
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