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UConn Health Department of Cell Biology

Lixia Yue

Lixia YueAssociate Professor
Department of Cell Biology

Education and Training

Ph.D., McGill University
Postdoctoral Fellow, Howard Hughes Medical Institute, Children's Hospital, Harvard Medical School

Contact

Phone: 860-679-3869
Fax: 860-679-1426
Email: lyue@uchc.edu
Office: ARB G024

UConn Health
263 Farmington Avenue
Farmington, CT 06030


Research Interests

Calcium is the most common signal transduction element in virtually all cells ranging from bacteria to neurons. Recent studies have demonstrated the importance of transient receptor potential (TRP) channels in mediating calcium signals. The mammalian TRP channel superfamily consists of a diverse group of calcium permeable nonselective cation channels that may play a role in pain transduction, thermo-sensation, mechanotransduction, tumor suppression, vasodilatation, and neurodegenerative disorder. Twenty-eight mammalian TRP channel genes have been cloned since the first TRP channel protein was identified in Drosophila , yet their physiological functions are to be revealed.

We are interested in calcium signaling mechanisms and their potential roles under physiological and pathological conditions. We apply a multidisciplinary approach to study the potential functions of the calcium-permeable TRP channels. We use molecular biology and biochemistry approaches to identify channel proteins and the associated partners; we use patch-clamp to study channel functions and gating mechanisms; and we use in vivo transgenic animal models to investigate physiological or pathological functions of the TRP channels.

Our current research projects include:

  1. TRP channels and calcium signaling mechanisms in cardiac fibrogenesis.
  2. Gating mechanism and physiological functions of TRPM7 and TRPM6, the two channel-kinase proteins that exhibit both channel functions and protein kinase activities.
  3. Gating mechanisms and potential roles of TRPM2

Selected Publications

Yue Z., Xie J., Yu A, Stock J, Du J, Yue L. Role of TRP channels in the cardiovascular system. Am J Physiol Heart Circ Physiol. 2015 Feb 1;308(3):H157-82. doi: 10.1152/ajpheart.00457.2014

Cagavi E, Bartulos O, Suh C, Sun B, Yue Z, Jiang Z, Yue L, Qyang Y. Functional cardiomyocytes derived from Isl1 cardiac progenitors via Bmp4 stimulation. PlosOne. 2014. Dec. 18.

Qin X, Yue Z, Sun B, Yang W, Xie J, Ni E, Feng Y, Mahmood R, Zhang Y, Yue L. Sphingosine and FTY720 are potent inhibitors of the transient receptor potential melastatin 7 (TRPM7) channels.  Br J Pharmacol. 2013 Mar;168(6):1294-312. (See commentary by Rohacs T. Sphingosine and the transient receptor potential channel kinase(s). Br J Pharmacol. 2013 Mar;168(6):1291-3).

Yue Z, Zhang Y, Xie J, Jiang J, Yue L.Transient Receptor Potential (TRP) channels and cardiac fibrosis.   Curr Top Med Chem. 2013 Feb 13. [Epub ahead of print].

Ge X, Ren Y, Bartulos O, Lee MY, Yue Z, Kim KY, Li W, Amos PJ, Bozkulak EC, Iyer A, Zheng W, Zhao H, Martin KA, Kotton DN, Tellides G, Park IH, Yue L, Qyang Y. Modeling supravalvular aortic stenosis syndrome with human induced pluripotent stem cells. Circulation. 2012; 126(14):1695-1704.

Lee MY, Sun B, Schliffke S, Yue Z, Ye M, Paavola J, Bozkulak EC, Amos PJ, Ren Y, Ju R, Jung YW, Ge X, Yue L, Ehrlich BE, Qyang Y.  Derivation of functional ventricular cardiomyocytes using endogenous promoter sequence from murine embryonic stem cells. Stem Cell Res. 2012;8(1):49-57

Estes NA 3rd, Sacco RL, Al-Khatib S, Ellinor P, Bezanson J, Alonso A, Antzelevitch C, Brockman RG, Chen P, Chugh S, Curtis A, Dimarco J, Ellenbogen K, Epstein A, Ezekowitz M, Fayad P, Gage B, Go A, Hlatky M, Hylek E, Jerosch-Herold M, Konstam M, Lee R, Packer D, Po SS, Prystowsky EN, Redline S, Rosenberg Y, Van Wagoner DR, Wood KA, Yue L, Benjamin EJ.  American Heart Association Atrial Fibrillation Research Summit: A Conference Report From the American Heart Association.  Circulation  2012 Oct 2;126(14):1695-704

Yue L, Xie J, Nattel S. Molecular determinants of cardiac fibroblast electrical function and therapeutic implications for atrial fibrillation. Cardiovasc Res. 2011; 89(4):744-53

Xie J, Sun B, Du J, Yang W, Chen HC, Overton JD, Runnels LW, Yue L. Phosphatidylinositol 4,5-bisphosphate (PIP(2)) controls magnesium gatekeeper TRPM6 activity. Sci Rep. 2011;1:146. P1-11. Epub 2011

Cover of Circulation ResearchDu J, Xie J, Silvermann D, Fusco D, Liang B, Yue L. TRPM7-Mediated Ca2+ Signals Confer Fibrogenesis in Human Atrial Fibrillation. Circulation Research. 2010; 106: 992-1003. (Featured on the cover of Circulation Research and was the first article by Editors’ pick)

Su LT, Chen HC, Gonzalez-Pagan O, Overton JD, Xie J, Yue L, Runnels LW. TRPM7 Activates m-Calpain by Stress-Dependent Stimulation of p38 MAPK and c-Jun N-Terminal Kinase. Journal of Molecular Biology. 2010; 396: 858-69

Du J, Xie J, Yue L. Modulation of TRPM2 by acidic pH and the underlying mechanisms for pH sensitivity. Journal of General Physiology. 2009; 134:471-488.

Heeringa S, Möller C, Du J, Yue L, Hinkes B1, Chernin G, Vlangos C, Hoyer P, Reiser J, and Hildebrandt F. A novel TRPC6 mutation in an early-onset family with FSGS strongly augments TRPC6 current amplitude. Plos One. 2009; 4:e7771.

Du J, Xie J, Yue L. Intracellular calcium activates TRPM2 and its alternative spliced isoforms. Proc Natl Acad Sci U S A. 2009; 107 (17) 1239-44.

Li M, Du J, Jiang J, Ratzan W, Su L-T, Runnels LW, Yue L. Molecular Determinants of Mg2+ and Ca2+ Permeability and pH Sensitivity in TRPM6 and TRPM7. J. Biol. Chem. 2007; 282(35):25817-25830.

Li M, Jiang J, Yue L. Functional characterization of homo- and heteromeric channel kinases TRPM6 and TRPM7. Journal of General Physiology. 2006 May;127(5):525-37.

Su L, Agapito M, Li, Simpson W, Huttenlocher A, Habas R, Yue L, Runnel R. TRPM7 regulates cell adhesion by controlling the calcium-dependent protease calpain. J Biol Chem. 2006 Apr 21;281(16):11260-70. Epub 2006 Jan 25.

Jiang J, Li M, Yue L. otentiation of TRPM7 inward currents by acidosis. Journal of General Physiology. 2005; 126 (2) 137-150.

*Runnels L, *Yue L, Clapham D. The TRP-Plik channel is inactivated by PIP2 hydrolysis. Nature Ce