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

The cAMP/PKA pathway rapidly activates SIRT1 to promote fatty acid oxidation independently of changes in NAD(+).
Authors: Authors: Gerhart-Hines Z, Dominy JE, Blättler SM, Jedrychowski MP, Banks AS, Lim JH, Chim H, Gygi SP, Puigserver P.
Mol Cell
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Myopathy caused by mammalian target of rapamycin complex 1 (mTORC1) inactivation is not reversed by restoring mitochondrial function.
Authors: Authors: Romanino K, Mazelin L, Albert V, Conjard-Duplany A, Lin S, Bentzinger CF, Handschin C, Puigserver P, Zorzato F, Schaeffer L, Gangloff YG, Rüegg MA.
Proc Natl Acad Sci U S A
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PGC1a promotes tumor growth by inducing gene expression programs supporting lipogenesis.
Authors: Authors: Bhalla K, Hwang BJ, Dewi RE, Ou L, Twaddel W, Fang HB, Vafai SB, Vazquez F, Puigserver P, Boros L, Girnun GD.
Cancer Res
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A hypoxia-induced positive feedback loop promotes hypoxia-inducible factor 1alpha stability through miR-210 suppression of glycerol-3-phosphate dehydrogenase 1-like.
Authors: Authors: Kelly TJ, Souza AL, Clish CB, Puigserver P.
Mol Cell Biol
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Clk2 and B56ß mediate insulin-regulated assembly of the PP2A phosphatase holoenzyme complex on Akt.
Authors: Authors: Rodgers JT, Vogel RO, Puigserver P.
Mol Cell
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Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming.
Authors: Authors: Dominy JE, Gerhart-Hines Z, Puigserver P.
Cold Spring Harb Symp Quant Biol
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Nuclear FoxO1 inflames insulin resistance.
Authors: Authors: Dominy JE, Puigserver P.
EMBO J
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Nutrient-dependent regulation of PGC-1alpha's acetylation state and metabolic function through the enzymatic activities of Sirt1/GCN5.
Authors: Authors: Dominy JE, Lee Y, Gerhart-Hines Z, Puigserver P.
Biochim Biophys Acta
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Conserved role of SIRT1 orthologs in fasting-dependent inhibition of the lipid/cholesterol regulator SREBP.
Authors: Authors: Walker AK, Yang F, Jiang K, Ji JY, Watts JL, Purushotham A, Boss O, Hirsch ML, Ribich S, Smith JJ, Israelian K, Westphal CH, Rodgers JT, Shioda T, Elson SL, Mulligan P, Najafi-Shoushtari H, Black JC, Thakur JK, Kadyk LC, Whetstine JR, Mostoslavsky R, Puigserver P, Li X, Dyson NJ, Hart AC, Näär AM.
Genes Dev
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Cdc2-like kinase 2 is an insulin-regulated suppressor of hepatic gluconeogenesis.
Authors: Authors: Rodgers JT, Haas W, Gygi SP, Puigserver P.
Cell Metab
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