Suneng FU

Suneng FU


Tsinghua University

 School of Life Sciences

 Principal Investigator


Education and Work Experience


1994-1998B.S. Dept. of Genetics, Fudan University.
TechnicianChinese Human Genome Center at Shanghai.
Ph.D. Dept. of Botany, Univ. of Georgia.
Postdoctoral FellowResearch 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 Area and Directions:


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.

1Regulatory 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.

2Translational 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.




2014  Awarded the Young Thousand Talent Program.


Selected Publication


Fu S, Yalcin A, Lee GY, Li P, Fan J, Arruda AP, Pers BM, Yilmaz M, Eguchi K, Hotamisligil GS. Phenotypic assays identify azoramide as a small-molecule modulator of the unfolded protein response with antidiabetic activity. Sci Transl Med. 2015, 7:292-98.

Fu S, Fan J, Blanco J, Gimenez-Cassina A, DanialNN, Watkins SM, HotamisligilGS. Polysome profiling in liver identifies dynamic regulation of endoplasmic reticulum translatome by obesity and fasting. PLoS Genet. 2012, 8:e1002902.  

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

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, 473:528-31.  

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, 11:467-78.




School of Life Sciences, Tsinghua University

Tsinghua University, Beijing 100084


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