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Tao Wang, M.D., Ph.D.
Associate Director, Medical Genetics Residency and Fellowship Program
Associate Professor of Pediatrics
Expertise: Medical Genetics
Research Interests: X-linked intellectual disability (XLID); Autism spectrum disorders (ASDs); Inborn errors of metabolism of central nerve system; Molecular basis of X-linked mental retardation and human cognitive development; Pathogenesis and therapy of inherited metabolic disease with CNS involvement ...read more
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Dr. Tao Wang is an associate professor of pediatrics at the Johns Hopkins University School of Medicine. His areas of clinical expertise include global developmental delays and intellectual disability neurobehavioral disorders in children, and genetic and genomic syndromes and inborn errors of metabolism.
Dr. Wang earned his M.D. from Zhongshan Medical University in China and a Ph.D. in human genetics from Johns Hopkins University. He completed his residency in pediatrics at Tufts -New England Medical Center Hospitals and performed fellowships in clinical genetics at Johns Hopkins University School of Medicine and clinical biochemical genetics at Kennedy Krieger Institute.
His research interests include x-linked intellectual disabilities (XLID), autism spectrum disorders (ASDs) and inborn errors of metabolism of the central nervous system.
Dr. Wang is the associate director of the Medical Genetics Residency and Fellowship Program and a preceptor in the Predoctoral Training Program in Human Genetics. He is certified by the American Board of Medical Genetics in Clinical Biochemical Genetics and Clinical Genetics.
- Associate Director, Medical Genetics Residency and Fellowship Program
- Associate Professor of Pediatrics
- MD, Peking Union Medical College Beijing (1987)
- Tufts -New England Medical Center Hospitals / Pediatrics (1999)
- Baylor College of Medicine / Cell Biology (1990)
- Johns Hopkins University School of Medicine / Pediatrics (2002)
- American Board of Medical Genetics / Clinical Genetics / MD (2002)
- American Board of Pediatrics / Pediatrics (1999)
Research & Publications
Our lab studies the genetic and neuronal mechanisms underlying developmental brain disorders including intellectual disability (ID) and autism spectrum disorders (ASDs) and in developing effective treatment for these disorders.
To systematically identify novel disease-causing genes for X-linked ID (XLID), we use high-throughput genomic approaches including X-chromosome cDNA microarray and next-generation sequencing to screen all known genes and functional elements on human X chromosome in XLID patients. We study mechanisms of novel XLID genes using in vitro and neuronal assays, electrophysiology and mutant mouse models. Current projects are focused on characterizing novel XLID candidate genes involving glutamate-signaling pathway, and phosphorylation and palmitoylation of key neuronal proteins.
To understand mechanisms of synaptic dysfunction in ASDs, we sequence genes encoding all known synaptic proteins, synaptome, in patients to identify causal and risk variants. We conduct functional studies of these variants using in vitro and neuronal assays, electrophysiology and mutant mouse models. One current focus is to understand glutamate-signaling disturbance in social dysfunction in ASDs.
Niranjan TS, May M, Skinner C, Turner T, Rose R, Stevenson R, Schwartz CE, Wang T. "Affected kindred analysis of human X chromosome exomes to identify novel X-linked intellectual disability genes" PLoS ONE. 2015 Feb 13;10(2):e0116454.
Ngoh A, Mctague A, Wentzensen IM, Meyer E, Applegate C, Kossoff EH, Batista DA, Wang T, Kurian MA. "Severe infantile epileptic encephalopathy due to mutations in PLCB1: expansion of the genotypic and phenotypic disease spectrum." Dev Med Child Neurol. 2014 Nov;56:1124-8.
Basehore MJ, Michaelson-Cohen R, Levy-Lahad E, Sismani C, Bird L, Friez MJ, Walsh TJ, Abidi F, Holloway L, Skinner C, McGee S, Alexandrou A, Syrrou M, Patsalis PC, Wang T, Schwartz CE, King MC, Stevenson RE. "Alpha-thalassemia intellectual disability: variable phenotypic expression among males with the p.R37X mutation." Clinic Genet. 2015 May;87(5):461-6.
Adamczyk A, Mejias R. Takamiya K, Yocum J, Krasnova N, Calderon J, Cadet JL, Huganir R, Pletnikov M, and Wang T (2012) "GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum." Behav Brain Res. 2012 Apr 1;229:265.
Pirooznia M, Wang T, Avramopoulos D, Valle D, Thomas G, Huganir R, Goes FS, Potash JB, Zandi PP. "SynaptomeDB: an ontology-based knowledgebase for synaptic genes." Bioinformatics. 2012 Mar 15;28(6):897.