Biosketch:

Dr. Yang received his BSc degree from Department of Chemistry, Zhejiang University in 1985 and his PhD in biochemistry and molecular biology from Shanghai Institute of Biochemistry, Chinese Academy of Sciences in May 1996. Afterwards, he Joined National Institutes of Health (NIH), USA for postdoctoral training. Since 1997, he has been a faculty member at McGill University, where he received tenure in 2003 and was promoted to a full professor in 2009.

His research at NIH and McGill University is focused on identification and functional analysis of histone acetyltransferases and deacetylases. At NIH, he identified the first two mammalian histone acetyltransferases, now known as KAT2A and KAT2B. His research team at McGill University identified MORF (MOZ-related factor, a.k.a. KAT6B), a human histone acetyltransferase paralogous to monocytic leukemia zinc finger protein (MOZ, a.k.a. KAT6A). Somatic KAT6A and KAT6B mutations have been implicated in leukemogenesis. His group has also identified and carried out molecular characterization of human histone deacetylases, including HDAC4. They demonstrated that HDAC4 interacts with MEF2 (myocyte enhancer factor 2) and functions as its transcriptional co-repressor. They also showed that 14-3-3 proteins bind to HDAC4 and regulate its nuclocytoplasmic trafficking in a signal-responsive manner, thereby uncovering a molecular mechanism through which extra- and intra-cellular signaling cues regulate histone (de)acetylation in the nucleus. In the past 10 years, his team has been generating and characterizing genetically modified mouse models lacking histone acetyltransferases or deacetylases, with a special focus on cerebral development. This line of research on mouse models has also led to expansion to related neurodevelopmental disorders. His team has recently identified and analyzed histone acetyltransferase and deacetylase gene mutations that cause multiple syndromic intellectual disability disorders.