Suneng FU,Ph.D

Principle Investigator, Assistant Professor

1994-1998,B.S. Dept. of Genetics, Fudan University.
1998-1999,Technician,Chinese Human Genome Center at Shanghai.
1999-2004,Ph.D. Dept. of Botany, Univ. of Georgia.
2004-2013,Postdoctoral Fellow,Research Associate, Dept. of Genetics and Complex Diseases, Harvard School of Public Health.
2013.6. Assistant Professor,School of Life Sciences, Tsinghua University, Peking-Tsinghua Center for Life Sciences.

Research interest

We study metabolism and metabolic diseases through integrated approaches of biochemistry, cell biology, and systems biology, for the purpose of dissecting their molecular mechanisms and developing their translational applications.  Our major focuses include the following related areas.

1)Regulatory mechanisms of metabolic organelle, specifically Endoplasmic Reticulum and mitochondria. Our lab has developed high-throughput and quantitative platforms for measuring ER and mitochondria function.  We will apply these platforms to systematically dissect genome-wide mechanisms governing organelle function and the potential roles of their dysfunction during the pathogenesis of obesity, aging and carcinogenesis.

2)Translational regulation of metabolism and organelle function. We developed ex-vivo platforms for translatomic analysis of mouse liver and other tissues.  We will apply this technology to study how translational regulation of metabolically important genes may impact cellular metabolism and organelle function.  Specifically, we will study how condition-specific regulation of alternative splicing and translational initiation may impact cellular metabolism and disease pathogenesis.

3) Network structure of metabolic regulation and system-level restoration. Current therapeutic strategies of metabolic diseases focus on individual pathways and specific proteins, and they do not have the capacity to restore cellular and organismal metabolism on a system level.  By integrating genome-wide experimentation with informatics and mathematic modeling, we hope to understand the mechanisms governing cellular metabolism and their network structures. Our eventual goal is to identify therapeutic strategies that will allow us to restore healthy metabolism on a genome- and whole-body level, and deliver sustainable benefits to our patients.



Selected publications

1: Fu S, Fan J, Blanco J, Gimenez-Cassina A, Danial NN, Watkins SM, Hotamisligil  GS. Polysome profiling in liver identifies dynamic regulation of endoplasmic reticulum translatome by obesity and fasting. PLoS Genet. 2012 Aug;8(8):e1002902.

2: Fu S, Watkins SM, Hotamisligil GS. The role of endoplasmic reticulum in hepatic lipid homeostasis and stress signaling. Cell Metab. 2012 May 2;15(5):623-34.

3: Fu S, Yang L, Li P, Hofmann O, Dicker L, Hide W, Lin X, Watkins SM, Ivanov AR, Hotamisligil GS. Aberrant lipid metabolism disrupts calcium homeostasis causing liver endoplasmic reticulum stress in obesity. Nature. 2011 May 26;473(7348):528-31.

4: Yang L, Li P, Fu S, Calay ES, Hotamisligil GS. Defective hepatic autophagy in  obesity promotes ER stress and causes insulin resistance. Cell Metab. 2010 Jun 9;11(6):467-78.

5: Jones MR, Quinton LJ, Blahna MT, Neilson JR, Fu S, Ivanov AR, Wolf DA, Mizgerd JP. Zcchc11-dependent uridylation of microRNA directs cytokine expression. Nat Cell Biol. 2009 Sep;11(9):1157-63


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