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

Interrupting synoviolin play at the ER: a plausible action to elevate mitochondrial energetics and silence obesity.
Authors: Authors: Soustek MS, Puigserver P.
EMBO J
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Adenosine activates thermogenic adipocytes.
Authors: Authors: Rines AK, Verdeguer F, Puigserver P.
Cell Res
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Genetic inhibition of hepatic acetyl-CoA carboxylase activity increases liver fat and alters global protein acetylation.
Authors: Authors: Chow JD, Lawrence RT, Healy ME, Dominy JE, Liao JA, Breen DS, Byrne FL, Kenwood BM, Lackner C, Okutsu S, Mas VR, Caldwell SH, Tomsig JL, Cooney GJ, Puigserver PB, Turner N, James DE, Villén J, Hoehn KL.
Mol Metab
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Targeting mitochondrial oxidative metabolism in melanoma causes metabolic compensation through glucose and glutamine utilization.
Authors: Authors: Lim JH, Luo C, Vazquez F, Puigserver P.
Cancer Res
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Cyclin D1-Cdk4 controls glucose metabolism independently of cell cycle progression.
Authors: Authors: Lee Y, Dominy JE, Choi YJ, Jurczak M, Tolliday N, Camporez JP, Chim H, Lim JH, Ruan HB, Yang X, Vazquez F, Sicinski P, Shulman GI, Puigserver P.
Nature
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USP7 attenuates hepatic gluconeogenesis through modulation of FoxO1 gene promoter occupancy.
Authors: Authors: Hall JA, Tabata M, Rodgers JT, Puigserver P.
Mol Endocrinol
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Cdc2-like kinase 2 suppresses hepatic fatty acid oxidation and ketogenesis through disruption of the PGC-1a and MED1 complex.
Authors: Authors: Tabata M, Rodgers JT, Hall JA, Lee Y, Jedrychowski MP, Gygi SP, Puigserver P.
Diabetes
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Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity.
Authors: Authors: Kraus D, Yang Q, Kong D, Banks AS, Zhang L, Rodgers JT, Pirinen E, Pulinilkunnil TC, Gong F, Wang YC, Cen Y, Sauve AA, Asara JM, Peroni OD, Monia BP, Bhanot S, Alhonen L, Puigserver P, Kahn BB.
Nature
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Decreased genetic dosage of hepatic Yin Yang 1 causes diabetic-like symptoms.
Authors: Authors: Verdeguer F, Blättler SM, Cunningham JT, Hall JA, Chim H, Puigserver P.
Mol Endocrinol
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Mitochondrial biogenesis through activation of nuclear signaling proteins.
Authors: Authors: Dominy JE, Puigserver P.
Cold Spring Harb Perspect Biol
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