Yingli Wang, DMD, PhD
- ADJUNCT ASSISTANT PROFESSOR | Genetics and Genomic Sciences
Yingli Wang, D.M.D., Ph.D., is an Assistant Professor of the Department of Genetics and Genomic Sciences at the Mount Sinai School of Medicine. Dr. Wang received her D.M.D. from at Xi’an Medical University, and a Master of Oral Pathology from Hubei Medical University, China. She received her Ph.D. in craniofacial biology from Peking University, China. She finished her postdoctoral training in craniofacial development and disorders at The Johns Hopkins University. She joined the Department of Genetics and Genomic Sciences at Mount Sinai School of Medicine as an instructor in 2007, and was promoted to Assistant Professor in 2010. Dr. Wang has given invited lectures in national and international conferences. She has served as reviewers for several journals including Molecular Medicine, Human Molecular Genetics and Experimental Cell Research.
DMD, Xi'an Medical University
MS, Hubei Medical University
PhD, Peking University
Johns Hopkins University
Craniosynostosis is a common malformation characterized by the premature closure of one or more of the cranial sutures of the skull. There are more than 100 human syndromes with craniosynostosis as a feature. Craniosynostosis can be caused by mutations in different genes including FGFR1, FGFR2, FGFR3, MSX2, TWIST1, EFNB1 and RAB23. Our research is focused on studying the pathogenesis, molecular mechanisms and pharmacologic treatment of human genetic malformations with craniosynostosis, including Apert, Beare-Stevenson cutis gyrate, Crouzon and Saethre-Chotzen syndromes, by creating and analyzing transgenic mouse models. We also study the developmental mechanisms of other craniofacial abnormalities including palate, choana, as well as long bone and visceral organs in these mouse models.
Wang Y, Xiao R, Yang F, Karim BO, Iacovelli AJ, Cai J, Lerner CP, Richtsmeier JT, Leszl JM, Hill CA, Yu K, Ornitz DM, Elisseeff J, Huso DL, Jabs EW. Abnormalities in cartilage and bone development in the Apert syndrome FGFR2(+/S252W) mouse. Development 2005 Aug; 132(15): 3537-3548.