Lixia Yue, Ph.D.Associate Professor, Department of Cell Biology
Calhoun Cardiology Center
|B.S.||Sun Yat-sen University,||Biology|
|M.S.||Sun Yat-sen University||Cardiovascular physiology|
|Ph.D.||McGill University School of Medicine||Cardiac electrophysiology|
|Postdoctoral||HARVARD MEDICAL SCHOOL||Electrophysiology & Molecular Biology|
|Name of Award/Honor||Awarding Organization|
|AHA-SDG award, 2003-2007||AHA|
|Postdoctoral fellowship award, Heart and Stroke Foundation of Canada, 1999-2001|
|Dean’s honor award for excellent PhD thesis|
|Studentship award, 1995-1999||Heart and Stroke Foundation of Canada|
|Name & Description||Category||Role||Type||Scope||Start Year||End Year|
|Editorial Board Member of Molecular Pharmacology||Editorial Board||Member||External||National||2013|
|Chartered member of NIH study section (ESTA)||Study Section||Member||External||National||2012||2016|
|Faculty of America Heart Association (FAHA)||Professional/Scientific Organization||Member||National||2012|
|Welcome Trust Foundation (United Kingdom)||Professional/Scientific Organization||Reviewer||External||National||2009|
|Founders (R1) study section||Study Section||Member||External||National||2008|
|National Institutes of Health, ESTA Study Section||Study Section||Member||External||National||2007|
|National Institutes of Health, ESTA Study Section,||Study Section||Member||External||National||2006|
|American Heart Association NEA3&4||Professional/Scientific Organization||Reviewer||External||National||2005||2007|
We are interested in Ca2+ signaling mechanisms and their potential roles under physiological and pathological conditions. 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 Ca2+ permeable nonselective cation channels that may play a role in pain transduction, thermo-sensation, mechanotransduction, tumor suppression, vasodilatation, and neurodegenerative disorder. More than 25 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 apply a multi-disciplinary approach to study the potential physiological and pathological functions of the Ca2+-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 animal models with disrupted or modified channel genes to investigate physiological or pathological functions of the TRP channels.
We currently focus on two major projects. First, we will investigate TRP channels and Ca2+ signaling mechanisms in cardiac fibrogenesis. Cardiac fibrosis is detrimental and is associated with a variety of heart diseases including arrhythmia, hypertrophy, and heart failure. However, Ca2+ signaling mechanism in cardiac fibrogenesis is unknown. This project will reveal potential roles of TRP channels in mediating Ca2+ signals in the cardiac fibroblast’s proliferation, differentiation, and fibrogenesis. Second, we are interested in the gating mechanisms and physiological functions of TRPM7 and TRPM6, the two channel-kinase proteins that exhibit both channel functions and protein kinase activities.
Accepting Lab Rotation Students: Summer '16, Fall '16, Spring '17
Lab Rotation Projects
Project #1: Potential physiological functions of TRPM7. We have recently found that TRPM7 is abundantly expressed in the heart (Nat. Cell. Biol. 2002). The goal of this project is to study how TRPM7 contributes to cardiac fibrogenesis, a pathological process that is involved in a variety of heart diseases including hypertrophy, heart failure and sudden cardiac death. For this project, the rotation student will start with studying how TRPM7 affects cardiac fibroblasts’ proliferation and differentiation.
Project #2: Gating mechanisms of TRPM7. A recent study showed that TRPM7 is responsible for neuronal cell death caused by anoxia. We have found that TRPM7 activity can be dramatically potentiated by ischemia related conditions (JGP, 2005. in press). This project is to identify the amino acid residues which determine the permeability, selectivity and gating mechanisms of TRPM7. Recombinant TRPM7 will be expressed in over-expression system and site-directed mutagenesis will be applied in this study. The ultimate goal of this project is to reveal the mechanism by which TRPM7 contributes to ischemic neuronal cell death and stroke.
Project #3: TRPV6 and Ca2+ signaling mechanism. TRPV6 (or CaT1) is the most Ca2+ selective ion channel in the TRP superfamily (Nature, 2001). Activation of TRPV6 requires lowered intracellular Ca2+ concentration. The objective of this project is to study how TRPM6 is gated under physiological conditions and potential roles of TRPV6 in Ca2+ signaling mechanism. Looking for interacting proteins with TRPV6 will be the first step for this project.