Pere Puigserver

Pere Puigserver, Ph.D.

Professor of Cell Biology (Dana-Farber Cancer Institute)
Professor of Cell Biology (HMS)

Pere Puigserver, Ph.D. is Professor of Cell Biology at Harvard Medical School and Dana-Farber Cancer Institute. He received his PhD in Biochemistry from UIB (Spain) that included research at Stockholm University, following postdoctoral work at the Dana-Farber Cancer Institute. He joined the faculty of Cell Biology at Johns Hopkins University School of Medicine in 2002 and subsequently returned in 2006 to the Department of Cell Biology (Harvard Medical School) and Cancer Biology (Dana-Farber Cancer Institute).

The Puigserver Lab focuses on the regulatory molecular mechanisms of core metabolic processes that maintain cell homeostasis and phenotypes. The research program of the Puigserver Lab includes main areas such as 1) mitochondrial biology, 2) intermediary metabolism and, 3) cancer metabolism and energetics. In mitochondrial biology, particular interests are in the regulatory mechanisms that control mitochondrial energetics and biogenesis, with implications in a variety of diseases including metabolic and mitochondrial diseases. In intermediary metabolism, a major focus is in liver and adipose cells and their regulatory mechanisms that control nutrient-derived metabolic and energetic activities. In cancer metabolism and energetics, the Puigserver Lab addresses how these processes drive core cancer biology programs such as cell growth, survival and resistance mechanisms.  The Puigserver Lab uses a multidisciplinary experimental design and approaches including chemical and genetic screens in mammalian cells, quantitative metabolomics and proteomics, biochemistry, mouse pre-clinical models of obesity/diabetes, mitochondrial diseases and cancer.    

Dana Farber Cancer Institute

Dept. of Cell Biology, LC-6213

360 Longwood Avenue

Boston, MA 02115

Lab telephone: 617-582-7977

Lab fax: 617-632-5363

Small molecules targeting selective PCK1 and PGC-1a lysine acetylation cause anti-diabetic action through increased lactate oxidation.
Authors: Authors: Mutlu B, Sharabi K, Sohn JH, Yuan B, Latorre-Muro P, Qin X, Yook JS, Lin H, Yu D, Camporez JPG, Kajimura S, Shulman GI, Hui S, Kamenecka TM, Griffin PR, Puigserver P.
Cell Chem Biol
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Structural basis of respiratory complex adaptation to cold temperatures.
Authors: Authors: Shin YC, Latorre-Muro P, Djurabekova A, Zdorevskyi O, Bennett CF, Burger N, Song K, Xu C, Paulo JA, Gygi SP, Sharma V, Liao M, Puigserver P.
Cell
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Feedforward cysteine regulation maintains melanoma differentiation state and limits metastatic spread.
Authors: Authors: Yu D, Liang J, Widlund HR, Puigserver P.
Cell Rep
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Structural basis of respiratory complexes adaptation to cold temperatures.
Authors: Authors: Shin YC, Latorre-Muro P, Djurabekova A, Zdorevskyi O, Bennett CF, Burger N, Song K, Xu C, Sharma V, Liao M, Puigserver P.
bioRxiv
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Tetracyclines activate mitoribosome quality control and reduce ER stress to promote cell survival.
Authors: Authors: Ronayne CT, Jackson TD, Bennett CF, Perry EA, Kantorovic N, Puigserver P.
EMBO Rep
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Selective Mitochondrial Respiratory Complex I Subunit Deficiency Causes Tumor Immunogenicity.
Authors: Authors: Liang J, Vitale T, Zhang X, Jackson TD, Yu D, Jedrychowski M, Gygi SP, Widlund HR, Wucherpfennig KW, Puigserver P.
bioRxiv
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A sweet way to regulate cellular growth: OGT and mTOR join forces.
Authors: Authors: Latorre-Muro P, Puigserver P.
Mol Cell
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Liver mitochondrial cristae organizing protein MIC19 promotes energy expenditure and pedestrian locomotion by altering nucleotide metabolism.
Authors: Authors: Sohn JH, Mutlu B, Latorre-Muro P, Liang J, Bennett CF, Sharabi K, Kantorovich N, Jedrychowski M, Gygi SP, Banks AS, Puigserver P.
Cell Metab
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Epigenetic suppression of PGC1a (PPARGC1A) causes collateral sensitivity to HMGCR-inhibitors within BRAF-treatment resistant melanomas.
Authors: Authors: Liang J, Yu D, Luo C, Bennett C, Jedrychowski M, Gygi SP, Widlund HR, Puigserver P.
Nat Commun
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Tetracycline-dependent inhibition of mitoribosome protein elongation in mitochondrial disease mutant cells suppresses IRE1a to promote cell survival.
Authors: Authors: Ronayne CT, Bennett CF, Perry EA, Kantorovich N, Puigserver P.
bioRxiv
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