Faculty Members

Dr. Xing-Zhen Chen

Professor
Department of Physiology
    Contact details are for academic matters only.

About Me

EMPLOYMENT AND TRAINING

Professor. 07/2011 –, Department of Physiology, University of Alberta, Canada.

Associate Professor. 07/2006 – 06/2011, Department of Physiology, University of Alberta.

Assistant Professor. 05/2000 – 06/2006, Department of Physiology, University of Alberta.

Instructor. 05/1999 – 05/2000, Harvard Medical School, USA.

Postdoctoral Fellow. 02/1997 – 05/1999, Brigham & Women’s Hospital, Harvard Medical School.

                                  Supervisor: Dr. Matthias A. Hediger.

Instructor. 08/1987 – 08/1991, Department of Biology, Zhejiang University, China.

EDUCATION

PhD in Physics. 09/1991 – 02/1997, Université de Montréal, Canada.

                              Supervisor: Dr. Jean-Yves Lapointe.

MSc in Physics. 09/1984 – 07/1987, Zhejiang University.

BSc in Physics. 02/1982 – 07/1984, Zhejiang University.

License candidate in Physics. 09/1981 02/1982, Université Pierre et Marie Curie - Paris VI, France.

DEUG A in Mathematics. 09/1979 07/1981, Université Claude Bernard - Lyon I, France.

French language learning. 02/1979 08/1979, Université de Rennes I, France.

BSc candidate in Computing Science. 10/1978 02/1979, Zhejiang University.

HONORS AND AWARDS

Senior Scholar, Alberta Heritage Foundation for Medical Research (AHFMR), 2006-2013.

Senior Scholar research prize, AHFMR, 2006-2013.

Research Award, Canada Foundation for Innovation New Opportunities (CFI NO).

Scholar, AHFMR, 2001-2006.

Scholar research prize, AHFMR, 2001-2006.

New Investigator, Canadian Institutes of Health Research (CIHR), 2000-2005.

Postdoctoral fellowship, International Human Frontier Science Program, 1998-2000.

Postdoctoral fellowship, Natural Sciences and Engineering Research Council of Canada (NSERC), 1998-2001, declined.

Awards of excellence, Université de Montréal, 1993 and 1994.


Teaching

"Molecular and Cellular Physiology", PHYSL 407/507, instructor and coordinator

"Physiology of Transport Systems", PHYSL 545,  instructor and coordinator

"Discovery Learning Pulmonary", DMED 514, facilitator

"Discovery Learning Renal", DMED 517, facilitator

"Undergraduate Research Project", PHYSL 467/468,  instructor and supervisor

"Mammalian and Human Physiology", PHYSL 210/211, instructor 

"Elementary Physiology", PHYSL 161,  instructor 

"Undergraduate Tutorial", PHYSL 466,  instructor 


Research

Cellular function and regulation of polycystins

Autosomal dominant polycystic kidney disease (ADPKD) is the most common form of PKD and occurs in 0.1-0.2% of adults. ADPKD is due to mutations in polycystin-1 and -2, which are membrane receptor and ion channel, respectively. ADPKD also leads to cysts in liver, pancreas and spleen, and to non-cystic manifestations, including vascular abnormalities, organ left-right asymmetry development, and hypertension. Other proteins, such as inversin, cystin, polaris, kinesin and tubulin, are also cystogenic in mice. At the cellular level, cystic epithelial cells show abnormalities in proliferation, differentiation, adhesion, polarity, fluid transport and apoptosis. The family of cystoproteins is also associated with other phenotypes, including fertility, mating behavior and muscle contraction, etc. Therefore, studies on polycystins may elucidate common molecular mechanisms underlying distinct physiological functions (phenotypes).

Polycystin-1 possesses a long extracellular N-terminus and acts as a receptor while polycystin-2 exhibits similar membrane organization to voltage-gated cation channels and transient receptor potential (TRP) channels. Polycystin-2 (also called PKD2 or TRPP2) and its homologue, polycystin-L (also called PKD2L1 or TRPP3), are non-selective cation channels, permeable to Ca, Na and K. Polycystin-L is not related to PKD. Increasing evidence indicates that polycystin-1 and -2 may be part of a mechano-sensor in epithelial cells while polycystin-L may be part of an acid sensor in neurons.

My laboratory studies function and regulation of polycystin-2 and -L, and interaction with other proteins, using molecular biology and cell physiology approaches, such as electrophysiology and protein-protein interaction, in combination with cellular and animal models. In particular, as project #1, we study cross-talk between polycystin-2 and cellular machineries related to translation or responses to stress conditions. As project #2, we try to determine functional roles of polycystin-L, in particular in neurons of retina and brain. 

Techniques

Molecular biology, protein-protein interaction, gene knockdown, immunostaining, mutagenesis, electrophysiology (patch-clamp, two-microelectrode voltage-clamp, and lipid bilayer reconstitution), radiotracer transport measurements, pulse chase, heterologous expression/purification of soluble and membrane proteins (in mammalian cells, E. coli and Xenopus oocytes), cell proliferation and apoptosis assays. Experimental models include Xenopus oocytes, cultured mammalian cells, zebrafish and mouse models


Research Keywords

Ion channel, electrophysiology, molecular biology, TRP channel, xenopus oocyte, culture cell, zebrafish, mouse, structure-function-regulation, protein-protein interaction, intramolecular interaction