BBS Faculty Member - Pere Puigserver

Pere Puigserver

Department of Cell Biology

Dana Farber Cancer Institute
Center for Life Sciences Building, 11-144
3 Blackfan Circle
Boston, MA 02115
Tel: 617-582-7745
Fax: 617-632-4770
Email: pere_puigserver@dfci.harvard.edu
Lab Members: 7 postdoctoral fellows, 2 graduate students
Visit my lab page here.



Our lab investigates broad aspects of fundamental metabolic and energetic processes in mammals that are necessary for cell survival and specific biological function. We combine and apply 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. As an example, we are pursuing chemical biology approaches to identify small compounds involved in nutrient sensing and metabolic reprogramming in a variety of mammalian cell types.

Studies from our group have identified new basic and evolutionary conserved metabolic circuitries within the PGC1 pathways 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. Our research program pursues fundamental biological and disease-relevant questions such as:

1- Nutrient Sensing and Cell Biology- What are the molecular components that sense and transmit nutrient signals to reprogram mammalian cells?
2- Mitochondrial Biology- What are the molecular components that sense signals to coordinate the supply of proteins for mitochondrial biogenesis, dynamics and function?
3- Cancer Metabolism- What are the genetic and epigenetic mechanisms underlying metabolic reprogramming and plasticity in tumor cells?



Last Update: 6/5/2014



Publications

For a complete listing of publications click here.

 


 

J.T. Cunningham, J.T. Rodgers, D. Arlow, F. Vazquez, V.K. Mootha and P. Puigserver. mTOR controls mitochondrial oxidative function through a YY1/PGC-1α complex Nature. 450, 736-740, 2007. http://www.ncbi.nlm.nih.gov/pubmed/18046414

S.M. Blättler, J.C. Cunningham, F. Verdeguer, H. Chim, W. Haas, M. Ruegg, H. Liu, S.P. Gygi, Y. Shi and P. Puigserver.Ying Yang 1 deficiency in skeletal muscle protects against rapamycin-induced diabetic-like symptoms through activation of insulin/IGF Signaling. Cell Metabolism. 4;15(4):505-17, 2012. http://www.ncbi.nlm.nih.gov/pubmed/22482732

F. Vazquez, J.H. Lim, H. Chim, K. Bhalla, G. Girnun, C.B. Clish, S.R. Granter, H.R. Windlund, B.M. Spiegelman and P. Puigserver. PGC1α expression defines a subset of human melanoma tumors with Increased mitochondrial capacity and resistance to oxidative stress. Cancer Cell. 23(3):287-301, 2013. http://www.ncbi.nlm.nih.gov/pubmed/23416000

Y. Lee, J.E. Dominy, Y.J. Choi, M. Jurczak, N. Tolliday, J.P. Camporez, H. Chim, J.H. Lim, H.B. Ruan, X. Yang, F. Vazquez, P. Sicinski, G.I. Shulman, P. Puigserver. Cyclin D1–Cdk4 controls glucose metabolism independently of cell cycle. progression. Nature (2014). In press, published online 25 May 2014. http://www.ncbi.nlm.nih.gov/pubmed/24870244



© 2013 by the President and Fellows of Harvard College