Title:
Zinc signaling in pathophysiology: Ten years later

 

Speaker:
Toshiyuki Fukada
Molecular and Cellular Physiology, Faculty of Pharmaceutical Sciences
Tokushima Bunri University
E-mail: fukada*ph.bunri-u.ac.jp 
HP: http://p.bunri-u.ac.jp/lab22/

 

Abstract:
Zinc is required for various cellular functions, and abnormal zinc homeostasis gives rise to health problems including skin disease, growth retardation, impaired bone homeostasis, neuronal dysfunctions, and immunodeficiency. Recent studies have provided further support for the important roles of zinc homeostasis in physiology and disease onset: zinc acts as a signaling mediator, recognized as “Zinc signaling”, controlled through zinc transporters. Advances of molecular, physiological, and genetic studies have accumulated evidences showing that zinc signaling participates in health and disease conditions by regulating many cellular events.
I will address zinc signaling contributes to maintain our health, by mainly highlighting the maintenance of epithelium, bone, connective tissues, and immunity, and discuss about “Zinc signal axis”; zinc signal selectively controls intracellular signaling and cellular events. With this realization that zinc signaling is a critical regulatory system of cellular signaling events, it will become a focus of attention for further understanding on the physiological role of zinc homeostasis and human disease.

 

Reference:
Zinc transporter SLC39A7/ZIP7 promotes intestinal epithelial self-renewal by resolving ER stress. PLOS Genetics 12: e1006349, 2016

SLC39A14 Is Required for the Development of Hepatocellular Iron Overload in Murine Models of Hereditary Hemochromatosis. Cell Metabolism 22: 138-150, 2015

Zinc transporter SLC39A10/ZIP10 facilitates anti-apoptotic signaling during early B-cell development. Proc Natl Acad Sci USA 111:11780-11785, 2014

Zinc transporter SLC39A10/ZIP10 controls humoral immunity by modulating B-cell receptor signal strength. Proc Natl Acad Sci USA 111:11786-11791, 2014

Molecular pathogenesis of Spondylocheirodysplastic Ehlers-Danlos syndrome caused by mutant ZIP13 proteins. EMBO Mol Med. 6: 1028-1042, 2014

Zinc Signals in Cellular Functions and Disorders, Edited by Fukada and Kambe: Springer, 2014