Dr. Yibin Wang
Molecular Signaling In Cardiac Diseases
BH 569, CHS
310-206-5197
yibinwang@mednet.ucla.edu 
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Research Interests:

Current research program evolves around the following three broad but integrated areas:
 
1. Signaling pathways and novel signaling molecules in cardiac myocytes stress responses. By applying state-of-the-art proteomic and functional genomic approaches,   we aim to identify the molecular components of the signaling pathways that mediate stress responses in cardiomyocytes.  We will use a large array of techniques to investigate their specific function in cardiac muscle cells and dissect out the signaling pathways responsible for the stress-induced changes in gene expression, cellular morphology, survival and apoptosis in cardiomyocytes.
2. Characterizing physiological significance of stress signaling in the development of heart failure. Using sophisticated transgenic and embryonic stem cell techniques, we have developed a number of novel animal models that have tissue-specific and temporally regulated perturbation of signaling pathways in the heart muscle cells. We will assess the cardiac phenotype of these animals at tissue, cellular, molecular and genomic levels. In addition, we will apply stress simulation to these animal models to simulate pathological conditions that trigger heart failure and investigate the role of these stress-signaling pathways in the process of the disease development.  
3. Physiological basis of heart failure at molecular and single cell levels. Using state-of-the-art imaging techniques, cellular and whole heart physiology tools, we will investigate the functional effects of specific stress signaling pathways on the fundamental cellular functions of the myocytes, including calcium homeostasis, excitation-contraction coupling, mitochondria regulation, intracellular trafficking, membrane organization and cell-cell communication. 
Our integrated approach from a broad range of experimental tools and both in vitro and in vivo model systems will help us to gain important insights to the mechanisms of a complex disease, such as heart failure. 

Representative Publications:

Liao P, Georgakopoulos D, Kovacs A, Zheng M, Lerner D, Pu H, Saffitz J, Chien K, Xiao RP, Kass DA, Wang Y. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy. Proc Natl Acad Sci U S A. 2001;98(21):12283-12288.

Takimoto E, Champion HC, Li M, Belardi D, Ren S, Rodriguez ER, Bedja D, Gabrielson KL, Wang Y, Kass DA. Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy. Nature Medicine. 2005;11(2):214-222.

Lu G, Kang YJ, Han J, Herschman HR, Stefani E, Wang Y. TAB-1 modulates intracellular localization of p38 MAP kinase and downstream signaling. J Biol Chem. 2006;281(9):6087-6095.

Synapse in Xenopus 
Nerve-muscle cell culture

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