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Pere Puigserver, PhD


Researcher

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Pere Puigserver, PhD

Researcher

  • Professor of Cell Biology, Harvard Medical School

Contact Information

  • Office Phone Number617-582-7977
  • Fax617-632-5363

Bio

Pere Puigserver is a Professor of Cell Biology at Harvard Medical School. His laboratory is based in the Department of Cancer Biology at Dana-Farber Cancer Institute, located in the Center for Life Sciences Boston (CLSB).

Dr. Puigserver received his B.S. in Biological Sciences and Ph.D. in Biochemistry at the University of Illes Balears, Spain. His graduate work focused on mitochondrial energetics using in-vitro and in-vivo approaches, and included research at the University of Stockholm. He pursued postdoctoral training in molecular and cellular biology at the Dana-Farber Cancer Institute and Harvard Medical School. In 2002, he was appointed Assistant Professor of Cell Biology at Johns Hopkins University School of Medicine. In 2006, he was recruited back to the Dana-Farber Cancer Institute and Harvard Medical School to continue his research program in cell metabolism.

Research

Nutrient Sensing, Mitochondrial Biology and Cancer Metabolism

The Puigserver Laboratory investigates broad aspects of fundamental metabolic and energetic processes in mammals that are necessary for cell survival and specific biological function. We focus on the molecular mechanisms by which mammalian cells sense, communicate, and respond to nutrients.

Studies from our group have identified new basic and evolutionary conserved metabolic circuitries that involve nutrient signaling to gene expression programs associated with cellular metabolic reprogramming. Components of these circuitries are dysregulated in metabolic diseases, cancer, and age-associated diseases and represent therapeutic targets.

The Lab’s research program pursues fundamental biological and disease-relevant questions such as:

  • What are the molecular components that sense and transmit nutrient signals to reprogram mammalian cells?
  • What are the molecular components that sense signals to coordinate the supply of proteins for mitochondrial biogenesis, dynamics, and function?
  • What are the genetic and epigenetic mechanisms underlying metabolic reprogramming and plasticity in tumor cells?

The Puigserver Lab’s research combines and applies a variety of biochemical, cellular, genetic, chemical biology, metabolic, and screening approaches both in cell culture and whole animals to identify the molecular mechanisms by which mammalian cells sense, communicate, and respond to nutrients. In particular, we have a close collaboration with the Broad Institute in chemical biology to identify small compounds involved in nutrient sensing and metabolic reprogramming in a variety of mammalian cell types.

 

Hypersensitivity to ferroptosis in chromophobe RCC is mediated by a glutathione metabolic dependency and cystine import via solute carrier family 7 member 11. Proc Natl Acad Sci U S A. 2022 07 12; 119(28):e2122840119.
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Mechanisms of mitochondrial respiratory adaptation. Nat Rev Mol Cell Biol. 2022 Jul 08.
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Atossa: a royal link between OXPHOS metabolism and macrophage migration. EMBO J. 2022 06 14; 41(12):e111290.
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Controversies surrounding peripheral cannabinoid receptor 1 in fatty liver disease. J Clin Invest. 2021 11 15; 131(22).
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Targeting adaptive cellular responses to mitochondrial bioenergetic deficiencies in human disease. FEBS J. 2021 Sep 12.
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Peroxisomal-derived ether phospholipids link nucleotides to respirasome assembly. Nat Chem Biol. 2021 06; 17(6):703-710.
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A cold-stress-inducible PERK/OGT axis controls TOM70-assisted mitochondrial protein import and cristae formation. Cell Metab. 2021 03 02; 33(3):598-614.e7.
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Tetracyclines promote survival and fitness in mitochondrial disease models. Nat Metab. 2021 01; 3(1):33-42.
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Structure-Activity Relationship and Biological Investigation of SR18292 (16), a Suppressor of Glucagon-Induced Glucose Production. J Med Chem. 2021 01 28; 64(2):980-990.
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Transcriptome-wide analysis of PGC-1a-binding RNAs identifies genes linked to glucagon metabolic action. Proc Natl Acad Sci U S A. 2020 09 08; 117(36):22204-22213.
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GCN5 acetyltransferase in cellular energetic and metabolic processes. Biochim Biophys Acta Gene Regul Mech. 2021 02; 1864(2):194626.
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Obesity/Type 2 Diabetes-Associated Liver Tumors Are Sensitive to Cyclin D1 Deficiency. Cancer Res. 2020 08 15; 80(16):3215-3221.
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Defective NADPH production in mitochondrial disease complex I causes inflammation and cell death. Nat Commun. 2020 06 01; 11(1):2714.
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H3K27me3-mediated PGC1a gene silencing promotes melanoma invasion through WNT5A and YAP. J Clin Invest. 2020 02 03; 130(2):853-862.
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Autophagy mediates hepatic GRK2 degradation to facilitate glucagon-induced metabolic adaptation to fasting. FASEB J. 2020 01; 34(1):399-409.
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Regulation of Hepatic Metabolism, Recent Advances, and Future Perspectives. Curr Diab Rep. 2019 09 07; 19(10):98.
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ER and Nutrient Stress Promote Assembly of Respiratory Chain Supercomplexes through the PERK-eIF2a Axis. Mol Cell. 2019 06 06; 74(5):877-890.e6.
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Inhibition of the ER stress IRE1a inflammatory pathway protects against cell death in mitochondrial complex I mutant cells. Cell Death Dis. 2018 05 31; 9(6):658.
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Insulin regulation of gluconeogenesis. Ann N Y Acad Sci. 2018 01; 1411(1):21-35.
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ERRa Maintains Mitochondrial Oxidative Metabolism and Constitutes an Actionable Target in PGC1a-Elevated Melanomas. Mol Cancer Res. 2017 10; 15(10):1366-1375.
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Selective Chemical Inhibition of PGC-1a Gluconeogenic Activity Ameliorates Type 2 Diabetes. Cell. 2017 03 23; 169(1):148-160.e15.
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Survival of tissue-resident memory T cells requires exogenous lipid uptake and metabolism. Nature. 2017 03 09; 543(7644):252-256.
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Adipose Tissue CLK2 Promotes Energy Expenditure during High-Fat Diet Intermittent Fasting. Cell Metab. 2017 02 07; 25(2):428-437.
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PGC-1 Coactivators: Shepherding the Mitochondrial Biogenesis of Tumors. Trends Cancer. 2016 10; 2(10):619-631.
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Bromodomain Inhibitors Correct Bioenergetic Deficiency Caused by Mitochondrial Disease Complex I Mutations. Mol Cell. 2016 10 06; 64(1):163-175.
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A PGC1a-mediated transcriptional axis suppresses melanoma metastasis. Nature. 2016 09 15; 537(7620):422-426.
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Targeting hepatic glucose metabolism in the treatment of type 2 diabetes. Nat Rev Drug Discov. 2016 11; 15(11):786-804.
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Breaking BRAF(V600E)-drug resistance by stressing mitochondria. Pigment Cell Melanoma Res. 2016 07; 29(4):401-3.
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The Methionine Transamination Pathway Controls Hepatic Glucose Metabolism through Regulation of the GCN5 Acetyltransferase and the PGC-1a Transcriptional Coactivator. J Biol Chem. 2016 May 13; 291(20):10635-45.
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Stem cells: Dietary fat promotes intestinal dysregulation. Nature. 2016 Mar 03; 531(7592):42-3.
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Oxidative Dimerization of PHD2 is Responsible for its Inactivation and Contributes to Metabolic Reprogramming via HIF-1a Activation. Sci Rep. 2016 Jan 07; 6:18928.
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Cancer Cells Hijack Gluconeogenic Enzymes to Fuel Cell Growth. Mol Cell. 2015 Nov 19; 60(4):509-11.
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Molecular pathophysiology of hepatic glucose production. Mol Aspects Med. 2015 Dec; 46:21-33.
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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity. Mol Cell Biol. 2015 Oct 26; 36(1):184-96.
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Interrupting synoviolin play at the ER: a plausible action to elevate mitochondrial energetics and silence obesity. EMBO J. 2015 Apr 15; 34(8):981-3.
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Adenosine activates thermogenic adipocytes. Cell Res. 2015 Feb; 25(2):155-6.
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Cyclin D1-Cdk4 controls glucose metabolism independently of cell cycle progression. Nature. 2014 Jun 26; 510(7506):547-51.
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Targeting mitochondrial oxidative metabolism in melanoma causes metabolic compensation through glucose and glutamine utilization. Cancer Res. 2014 Jul 01; 74(13):3535-45.
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Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014 Apr 10; 508(7495):258-62.
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USP7 attenuates hepatic gluconeogenesis through modulation of FoxO1 gene promoter occupancy. Mol Endocrinol. 2014 Jun; 28(6):912-24.
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Genetic inhibition of hepatic acetyl-CoA carboxylase activity increases liver fat and alters global protein acetylation. Mol Metab. 2014 Jul; 3(4):419-31.
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Decreased genetic dosage of hepatic Yin Yang 1 causes diabetic-like symptoms. Mol Endocrinol. 2014 Mar; 28(3):308-16.
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Cdc2-like kinase 2 suppresses hepatic fatty acid oxidation and ketogenesis through disruption of the PGC-1a and MED1 complex. Diabetes. 2014 May; 63(5):1519-32.
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Mitochondrial biogenesis through activation of nuclear signaling proteins. Cold Spring Harb Perspect Biol. 2013 Jul 01; 5(7).
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The sirtuin family's role in aging and age-associated pathologies. J Clin Invest. 2013 Mar; 123(3):973-9.
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PGC1a expression defines a subset of human melanoma tumors with increased mitochondrial capacity and resistance to oxidative stress. Cancer Cell. 2013 Mar 18; 23(3):287-301.
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Oleic acid stimulates complete oxidation of fatty acids through protein kinase A-dependent activation of SIRT1-PGC1a complex. J Biol Chem. 2013 Mar 08; 288(10):7117-26.
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In vivo measurement of the acetylation state of sirtuin substrates as a proxy for sirtuin activity. Methods Mol Biol. 2013; 1077:217-37.
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The deacetylase Sirt6 activates the acetyltransferase GCN5 and suppresses hepatic gluconeogenesis. Mol Cell. 2012 Dec 28; 48(6):900-13.
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TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis. Cell. 2012 Sep 28; 151(1):96-110.
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A metabolic prosurvival role for PML in breast cancer. J Clin Invest. 2012 Sep; 122(9):3088-100.
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Defective mitochondrial morphology and bioenergetic function in mice lacking the transcription factor Yin Yang 1 in skeletal muscle. Mol Cell Biol. 2012 Aug; 32(16):3333-46.
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Yin Yang 1 deficiency in skeletal muscle protects against rapamycin-induced diabetic-like symptoms through activation of insulin/IGF signaling. Cell Metab. 2012 Apr 04; 15(4):505-17.
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Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming. Cold Spring Harb Symp Quant Biol. 2011; 76:203-9.
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Glycine decarboxylase cleaves a "malignant" metabolic path to promote tumor initiation. Cancer Cell. 2012 Feb 14; 21(2):143-5.
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The cAMP/PKA pathway rapidly activates SIRT1 to promote fatty acid oxidation independently of changes in NAD(+). Mol Cell. 2011 Dec 23; 44(6):851-63.
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Myopathy caused by mammalian target of rapamycin complex 1 (mTORC1) inactivation is not reversed by restoring mitochondrial function. Proc Natl Acad Sci U S A. 2011 Dec 20; 108(51):20808-13.
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PGC1a promotes tumor growth by inducing gene expression programs supporting lipogenesis. Cancer Res. 2011 Nov 01; 71(21):6888-98.
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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. Mol Cell Biol. 2011 Jul; 31(13):2696-706.
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Clk2 and B56ß mediate insulin-regulated assembly of the PP2A phosphatase holoenzyme complex on Akt. Mol Cell. 2011 Feb 18; 41(4):471-9.
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Nuclear FoxO1 inflames insulin resistance. EMBO J. 2010 Dec 15; 29(24):4068-9.
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Conserved role of SIRT1 orthologs in fasting-dependent inhibition of the lipid/cholesterol regulator SREBP. Genes Dev. 2010 Jul 01; 24(13):1403-17.
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Cdc2-like kinase 2 is an insulin-regulated suppressor of hepatic gluconeogenesis. Cell Metab. 2010 Jan; 11(1):23-34.
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Nutrient-dependent regulation of PGC-1alpha's acetylation state and metabolic function through the enzymatic activities of Sirt1/GCN5. Biochim Biophys Acta. 2010 Aug; 1804(8):1676-83.
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Foxo1 integrates insulin signaling with mitochondrial function in the liver. Nat Med. 2009 Nov; 15(11):1307-11.
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Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment. Nature. 2009 Sep 03; 461(7260):109-13.
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GCN5-mediated transcriptional control of the metabolic coactivator PGC-1beta through lysine acetylation. J Biol Chem. 2009 Jul 24; 284(30):19945-52.
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AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity. Nature. 2009 Apr 23; 458(7241):1056-60.
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Insulin resistance: beta-arrestin development. Cell Res. 2009 Mar; 19(3):275-6.
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A PGC-1alpha-O-GlcNAc transferase complex regulates FoxO transcription factor activity in response to glucose. J Biol Chem. 2009 Feb 20; 284(8):5148-57.
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Concurrent regulation of AMP-activated protein kinase and SIRT1 in mammalian cells. Biochem Biophys Res Commun. 2009 Jan 23; 378(4):836-41.
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The genetic ablation of SRC-3 protects against obesity and improves insulin sensitivity by reducing the acetylation of PGC-1{alpha}. Proc Natl Acad Sci U S A. 2008 Nov 04; 105(44):17187-92.
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O-GlcNAc regulates FoxO activation in response to glucose. J Biol Chem. 2008 Jun 13; 283(24):16283-92.
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Metabolic Adaptations Through PGC-1α and SIRT1 Pathways. FEBS Letters. 2008; 582:46-53.

mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex. Nature. 2007 Nov 29; 450(7170):736-40.
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Metabolic adaptations through the PGC-1 alpha and SIRT1 pathways. FEBS Lett. 2008 Jan 09; 582(1):46-53.
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Fasting-dependent glucose and lipid metabolic response through hepatic sirtuin 1. Proc Natl Acad Sci U S A. 2007 Jul 31; 104(31):12861-6.
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SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis. EMBO J. 2007 Jul 11; 26(13):3169-79.
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Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC-1alpha. EMBO J. 2007 Apr 04; 26(7):1913-23.
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Receptor feasts on sugar and cholesterol. Nat Med. 2007 Feb; 13(2):128-9.
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Mammalian Metabolism in Aging. Molecular Biology of Aging. Edited by L. Guarente, L. Partridge and D.C. Wallace. Cold Spring Harbor Monograph Series. 2007; 51.

Fasting-Dependent Glucose and Lipid Metabolic Response through Hepatic SIRT1. Proc. Natl. Acad. Sci. USA. 2007; 104(31):12861-66.

Metabolic Control of Mitochondrial Function and Fatty Acid Oxidation Through PGC-1α/SIRT1. EMBO J. 2007; 26:1913-1923.

mTOR controls mitochondrial oxidative function through a YY1/PGC-1α complex. Nature. 2007; 450:736-740.

Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell. 2006 Dec 15; 127(6):1109-22.
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Resveratrol improves health and survival of mice on a high-calorie diet. Nature. 2006 Nov 16; 444(7117):337-42.
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Hypothalamic malonyl-CoA triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle: Role of PGC-1alpha. Proc Natl Acad Sci U S A. 2006 Oct 17; 103(42):15410-5.
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Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction. J Biol Chem. 2006 Aug 04; 281(31):21745-21754.
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GCN5 acetyltransferase complex controls glucose metabolism through transcriptional repression of PGC-1alpha. Cell Metab. 2006 Jun; 3(6):429-38.
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Certainly can't live without this: SIRT6. Cell Metab. 2006 Feb; 3(2):77-8.
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Certainly you can’t live without it: SIRT6. Cell Metabolism. 2006; 3(2):77-8.

Hypothalamic malonyl-CoA triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle: Role of PGC-1α. Proc. Natl. Acad. Sci. 2006; 103(42):15410-5.

Resveratrol promotes mitochondrial biogenesis and protects against metabolic disease through activating SIRT1 and PGC-1α activity. Cell. 2006; 127(6):1109-22.

Foxa2, a novel transcriptional regulator of insulin sensitivity. Nat Med. 2006 Jan; 12(1):38-9.
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Modulators of cdc2-like kinases (CLKs) and methods of use thereof. 2005.

Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. Nature. 2005 Mar 03; 434(7029):113-8.
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Tissue-specific regulation of metabolic pathways through the transcriptional coactivator PGC1-alpha. Int J Obes (Lond). 2005 Mar; 29 Suppl 1:S5-9.
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Nutrient Control of Gluconeogenesis Through PGC-1α/SIRT1 Deacetylase Complex. Nature. 2005; 434:113-8.

Tissue-Specific Regulation of Metabolic Pathways Through the Transcriptional Coactivator PGC-1α. Int. J. Obes. Relat. Metab. Disord. 2005; 29:S5-9.

Erralpha and Gabpa/b specify PGC-1alpha-dependent oxidative phosphorylation gene expression that is altered in diabetic muscle. Proc Natl Acad Sci U S A. 2004 Apr 27; 101(17):6570-5.
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p38 mitogen-activated protein kinase is the central regulator of cyclic AMP-dependent transcription of the brown fat uncoupling protein 1 gene. Mol Cell Biol. 2004 Apr; 24(7):3057-67.
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Suppression of mitochondrial respiration through recruitment of p160 myb binding protein to PGC-1alpha: modulation by p38 MAPK. Genes Dev. 2004 Feb 01; 18(3):278-89.
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Suppression of Mitochondrial Respiration via p160 Myb Binding Protein Docking on PGC-1α: Modulation by p38 MAPK. Genes Dev. 2004; 18:278-289.

ERRalpha and Gabpa/b specify PGC-1alpha-dependent oxidative phosphorylation gene expression that is altered in diabetic muscle. Proc. Natl. Acad. Sci. USA. 2004; 101:6570-5.

p38 Mitogen-Activated Protein Kinase is the Central Regulator of cAMP-Dependent Transcription of the Brown Fat Uncoupling Protein 1 Gene. Mol.Cell Biol. 2004; 24:3057-3067.

PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes. Nat Genet. 2003 Jul; 34(3):267-73.
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Suppression of beta cell energy metabolism and insulin release by PGC-1alpha. Dev Cell. 2003 Jul; 5(1):73-83.
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PGC-1beta in the regulation of hepatic glucose and energy metabolism. J Biol Chem. 2003 Aug 15; 278(33):30843-8.
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Insulin-regulated hepatic gluconeogenesis through FOXO1-PGC-1alpha interaction. Nature. 2003 May 29; 423(6939):550-5.
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Regulation of hepatic fasting response by PPARgamma coactivator-1alpha (PGC-1): requirement for hepatocyte nuclear factor 4alpha in gluconeogenesis. Proc Natl Acad Sci U S A. 2003 Apr 01; 100(7):4012-7.
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Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha): transcriptional coactivator and metabolic regulator. Endocr Rev. 2003 Feb; 24(1):78-90.
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Characterization of the peroxisome proliferator activated receptor coactivator 1 alpha (PGC 1alpha) expression in the murine brain. Brain Res. 2003 Jan 31; 961(2):255-60.
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PGC-1α: Metabolic Regulator and Transcriptional Coactivator. Endocr. Rev. 2003; 24(1):78-90.

Insulin-Regulated Hepatic Gluconeogenesis Through FOXO1/PGC-1α Interaction. Nature. 2003; 423:550-5.

Regulation of hepatic fasting response by PPARgamma coactivator-1 alpha (PGC-1): Requirement for hepatocyte nuclear factor 4 alpha in gluconeogenesis. Proc. Natl. Acad. Sci. USA. 2003; 100:4012-7.

Suppression of β-Cell Energy Metabolism and Insulin release by PGC-1α. Dev. Cell. 2003; 5:73-83.

Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres. Nature. 2002 Aug 15; 418(6899):797-801.
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PGC-1β: A novel transcription coactivator associated with host cell factor. J. Biol. Chem. 2002; 277:1645-1648.

Transcriptional Co-activator PGC-1α drives the formation of slow-twitch muscle fibers. Nature. 2002; 418:797-801.

Peroxisome proliferator-activated receptor gamma coactivator 1beta (PGC-1beta ), a novel PGC-1-related transcription coactivator associated with host cell factor. J Biol Chem. 2002 Jan 18; 277(3):1645-8.
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Cytokine stimulation of energy expenditure through p38 MAP kinase activation of PPARgamma coactivator-1. Mol Cell. 2001 Nov; 8(5):971-82.
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CREB regulates hepatic gluconeogenesis through the coactivator PGC-1. Nature. 2001 Sep 13; 413(6852):179-83.
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Control of hepatic gluconeogenesis through the transcriptional coactivator PGC-1. Nature. 2001 Sep 13; 413(6852):131-8.
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Restoration of insulin-sensitive glucose transporter (GLUT4) gene expression in muscle cells by the transcriptional coactivator PGC-1. Proc Natl Acad Sci U S A. 2001 Mar 27; 98(7):3820-5.
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CREB Regulates Hepatic Gluconeogenesis via the Co-activator PGC-1. Nature. 2001; 413:179-183.

Cytokine-Activation of Energy Expenditure through p38 MAP kinase phosphorylation of the PPARγ coactivator (PGC-1). Mol. Cell. 2001; 8:971-982.

Restoration of Insulin-Sensitive Glucose Transporter (GLUT-4) Gene Expression in Muscle Cells by the Transcriptional Coactivator PGC-1. Proc. Natl. Acad. Sci. 2001; 98:3820-3825.

Regulation of adipogenesis and energy balance by PPARgamma and PGC-1. Int J Obes Relat Metab Disord. 2000 Nov; 24 Suppl 4:S8-10.
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Direct coupling of transcription and mRNA processing through the thermogenic coactivator PGC-1. Mol Cell. 2000 Aug; 6(2):307-16.
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Transcriptional regulation of adipogenesis. Genes Dev. 2000 Jun 01; 14(11):1293-307.
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Modulation of estrogen receptor-alpha transcriptional activity by the coactivator PGC-1. J Biol Chem. 2000 May 26; 275(21):16302-8.
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Regulation of adipogenesis and energy balance by PPARγ and PGC-1. Int. J. Obes. Relat. Metab. Disord. 2000; 24(4):S8-10.

Transcriptional activation of adipogenesis. Curr Opin Cell Biol. 1999 Dec; 11(6):689-94.
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Activation of PPARgamma coactivator-1 through transcription factor docking. Science. 1999 Nov 12; 286(5443):1368-71.
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Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1. Cell. 1999 Jul 09; 98(1):115-24.
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Stimulation of uncoupling protein 1 expression in brown adipocytes by naturally occurring carotenoids. Int J Obes Relat Metab Disord. 1999 Jun; 23(6):650-5.
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Regulation of energy balance by PPARγ and its coactivators. Progress in Obesity Research. Edited by B. Guy-Grand and G. Ailhaud. 1999; 39-46.

Stimulation of uncoupling protein 1 expression in brown adipocyte by naturally occurring carotenoids. Int. J. Obes. Relat. Metab. Disord. 1999; 23:650-5.

Activation of PPARγ Coactivator (PGC-1) Through Transcription Factor Docking. Science. 1999; 286(5443):1368-71.

2-Methoxyestradiol, an endogenous metabolite of 17beta-estradiol, inhibits adipocyte proliferation. Mol Cell Biochem. 1998 Dec; 189(1-2):1-7.
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Involvement of the retinoblastoma protein in brown and white adipocyte cell differentiation: functional and physical association with the adipogenic transcription factor C/EBPalpha. Eur J Cell Biol. 1998 Oct; 77(2):117-23.
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PGC-1alpha. Novel Brown Fat PPARgamma coactivator. 1998.

A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis. Cell. 1998 Mar 20; 92(6):829-39.
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2-Methoxyoestradiol, an endogenous metabolite of 17-β-estradiol, inhibits adipocyte proliferation. Mol. Cell. Biochem. 1998; 189:1-7.

Diminished response to food deprivation of the rat brown adipose tissue mitochondrial uncoupling system with age. Biochem Mol Biol Int. 1997 Sep; 42(6):1151-61.
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Retinoic acid modulates retinoid X receptor alpha and retinoic acid receptor alpha levels of cultured brown adipocytes. FEBS Lett. 1997 Apr 07; 406(1-2):196-200.
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Diminished response to food deprivation of the rat brown adipose tissue mitochondrial uncoupling system with age. Biochem. Mol. Biol. Int. 1997; 42:1151-1161.

Retinoic acid modulates RARα and RXRα levels in cultured brown adipocytes. FEBS Lett. 1997; 406:196-200.

In vitro and in vivo induction of brown adipocyte uncoupling protein (thermogenin) by retinoic acid. Biochem J. 1996 Aug 01; 317 ( Pt 3):827-33.
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Effect of selective beta-adrenoceptor stimulation on UCP synthesis in primary cultures of brown adipocytes. Mol Cell Endocrinol. 1996 Mar 01; 117(1):7-16.
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Effect of selective ß-adrenoceptor stimulation on UCP expression in primary cultures of brown adipocytes. Mol. Cell Endocrinol. 1996; 117:7-16.

In vitro an in vivo induction of the uncoupling protein thermogenin by retinoids. Biochem. J. 1996; 317:827-833.

Cold exposure induces different uncoupling-protein thermogenin masking/unmasking processes in brown adipose tissue depending on mitochondrial subtypes. Biochem J. 1994 Jun 01; 300 ( Pt 2):463-8.
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Dietary regulation of fasting-induced mitochondrial protein degradation in adult rat brown adipose tissue. Biochem Int. 1992 Sep; 27(6):1037-46.
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Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool. Biochem J. 1992 Jun 01; 284 ( Pt 2):393-8.
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Impaired starvation-induced loss of mitochondrial protein in the brown adipose tissue of dietary obese rats. Int J Obes Relat Metab Disord. 1992 Apr; 16(4):255-61.
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Impaired starvation-induced loss of mitochondrial protein in the brown adipose tissue of dietary obese rats. Int. J. Obes. 1992; 16:255-261.

Adrenergic stimulation and obesity status regulate induction and degradation of the thermogenic uncoupling protein in brown adipose in-vitro and in-vivo. 1992.

Evidence for masking of brown adipose tissue mitochondrial GDP-binding sites in response to fasting in rats made obese by dietary manipulation. Effects of reversion to standard diet. Biochem J. 1991 Oct 15; 279 ( Pt 2):575-9.
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Adrenergic regulation of differentiation and proliferation in brown adipocyte cultures. Obesity in Europe. Edited by G. Ailhaud et al. 1991; 355-361.

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