Meng Wu received his PhD in Biochemistry and Molecular Biology from Peking Union Medical College in China, studying chromatin remodeling in neural differentiation. He had his postdoctoral training in the Center for Molecular Cardiology at Mount Sinai, focusing on the functions of epigenetic regulators in the formation of the cardiac conduction system. He is currently an Instructor in Dr. Ethylin Wang Jabs’ group studying molecular mechanisms of human malformation disorders including craniosynostosis, neural tube defects and Roberts syndrome.
Bone Biology, Cartilage Biology, Cellular Differentiation, Chromatin, Developmental Biology, Epigenetics, Epigenomics, Gene Regulation, Genetics, Knockout Mice, Molecular Biology, Stem Cells, Structural Biology, Systems Biology
Postdoctoral Fellow, Icahn School of Medicine at Mount Sinai
BS, Zhejiang University
PhD, Peking Union Medical College
Craniosynostosis Network is an organized and synergistic research program to understand the genetic basis and developmental mechanism of craniosynostosis (http://labs.icahn.mssm.edu/peterlab/craniosynostosis-network/). Project III: Systems Biology of Bone in Coronal Nonsyndromic Craniosynostosis We generate and differentiate patient-derived iPS cells and analyze the transcriptomic profiles during osteogenic differentiation to study systems biology of coronal nonsyndromic craniosynostosis (cNSC). An in vitro osteogenic differentiation model has been developed and high-throughput RNA-seq datasets on human normal and cNSC mesenchymal cells, preosteoblasts and osteoblasts are used to capture the genetic regulation of gene expression and guide network construction.
Folate Pathway and Neural Tube Defects
Neural tube defects (NTDs) are birth defects of the brain and spinal cord. They are a major cause of death and lifelong disability worldwide. Folic acid is known to reduce the risk of a pregnancy being affected by a neural tube defect but it is unclear how folate metabolism is involved in neural tube development. Folate responsive and non-folate responsive NTD mouse models are used for transcriptome and epigenome profiling in neural tubes to explore the molecular pathogenesis of folate pathway-related NTDs.
Study of the Limb Defects in Roberts Syndrome
Roberts syndrome (RBS) is a rare genetic disorder characterized by limb and facial abnormalities. RBS is caused by mutations in the ESCO2 gene, which encodes a protein belonging to the Eco1/Ctf7 family of acetyltransferases. We are using an Esco2 conditional knock out mouse model as well as patient-derived iPS cells to study the limb reduction defects in this syndrome and the pathogenic mechanism of mutant ESCO2.
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Dr.Wu did not report having any of the following types of financial relationships with industry during 2018 and/or 2019: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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