Research

John H. White

John H. White

Title:   
Professor 

Institute:
McGill University, Montreal

Department:  
Physiology

Province:
Quebec

Training:  
PhD, Biochemistry, Harvard University, Cambridge, MA, USA   
MSc, Chemistry, Carleton University, Ottawa, Ontario, Canada
BSc, Biochemistry, Carleton University, Ottawa, Ontario, Canada
 
Research interests:
Vitamin D, cancer chemoprevention, regulation of innate immunity

Career highlights:
Identification of the nuclear receptor coregulator LCoR; discovery that the active form of vitamin D is a direct inducer of antimicrobial innate immunity in humans; discovery that the active form of vitamin D stimulates the function of tumor suppressors and longevity factors FoxO proteins and Sirt1.
 

Research Projects

Project title:
Functional interactions of the vitamin D receptor with Class III histone deacetylase Sirtuin 1

Funding period:  
2010-2012

Program:
Operating Grant (Environment-cancer)

Summary:
Population-based studies provide clear correlations between vitamin D insufficiency and the prevalence of several cancers, particularly those of the digestive tract, consistent with chemopreventive effects of vitamin D. The active form of vitamin D interacts with the vitamin D receptor (VDR). We have found that the VDR regulates the function of a protein called sirtuin 1 (Sirt1), which is important for prevention of cancers of the digestive tract. We are interested in understanding the functional consequences of the interaction of the VDR with Sirt 1.

CRS publications:

An, B.-S., Tavera-Mendoza, L.E., Dimitrov, V., Wang, X., Calderon, M., Wang, H.-J., and White, J.H. (2010) Stimulation of SIRT1-regulated FoxO protein function by the ligand-bound vitamin D receptor. Mol. Cell. Biol. 30, 4890-4900.

Past CRS projects:

2005 Molecular mechanisms underlying the antiproliferative effects of vitamin D3 in cancer cells

1999 Analysis of the molecular mechanisms of growth inhibition of breast cancer cells by 1,25-dihydroxyvitamin D3. Identification of novel D3-regulated genes.