Guangju Ji
Professor
Institute of Biophysics
Chinese Academy of Sciences
China
Biography
1978-1983 The Forth Military Medical University,M.D. 1988-1991  The Forth Military Medical University,M.S. (Pharmacology) 1994-1999  University of Cologne, Germany, Ph.D., (physiology) 1999-2001  University of Pennsylvania US, Postdoctoral Fellow 2001-2004  Cornell University, Dept. of Biomedical Sciences, Research Assistant Prof. 2004-2006  Cornell University, Dept. of Biomedical Sciences, Research Associate Prof 2006-    Investigator, Institute of Biophysics, Chinese Academy of Sciences
Research Interest
My laboratory focuses on the molecular processes underlying excitation-contraction coupling, integration /modulation of Ca2+ signaling in vivo, as well as the roles and mechanisms of Ca2+ homeostasis disturbance-caused diseases. Current studies seek to understand the role of the specific sarcoplasmic/endoplasmic reticular calcium release channels, the sarcolemmal ion channels and their regulatory proteins in cellular excitation-contraction coupling. A major goal of the laboratory is to understand the processes of intercellular communication and the generation of spontaneous Ca2+ signal activity and the mechanisms of Ca2+ signaling disturbance causing diseases related. Projects in the laboratory include the study of the molecular mechanism of the Ca2+ signaling disturbance, the development and progress of related diseases induced by intracellular Ca2+ homeostasis disturbance, identification of genes encoding channel regulatory proteins and relating signaling molecules involved in muscle biology and determination of the extent to which these genes are altered in specific disease processes, and the development of genetically encoded sensors of cell signaling. An additional effort in the laboratory is to combine molecular design, electrophysiology and advanced optical imaging technologies to advance the understanding of path- physiological processes, destination, functions, integration with host tissues /organs of implanted ESC derived cells for treatment of injured organ function.
Publications
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3. Zhang Q, Jiang J, Han P, Yuan Q, Zhang J, Zhang X, Xu Y, Cao H, Meng Q, Chen L, Tian T, Wang X, Li P, Hescheler J, Ji G*, Ma Y. Direct differentiation of atrial and ventricular myocytes from human embryonic stem cells by alternating retinoid signals. Cell Res. 2011 Apr;21(4):579-87.
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2. Zhang X, Tallini YN, Chen Z, Gan L, Wei B, Doran R, Miao L, Xin HB, Kotlikoff MI, Ji G*. Dissociation of FKBP12.6 from ryanodine receptor type 2 is regulated by cyclic ADP-ribose but not beta-adrenergic stimulation in mouse cardiomyocytes. Cardiovasc Res. 2009 Nov 1;84(2):253-62.
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1. Chen Z, Li Z, Wei B, Yin W, Xu T, Kotlikoff MI,Ji G*. FKBP12.6-knockout mice display hyperinsulinemia and resistance to high-fat diet-induced hyperglycemia. FASEB J. 2010 ; 24(2):357-63.