Graph of clinical severity score of multiple sclerosis over 40 days after immunization for wild type and HDAC11 knock out mice.
Loss of HDAC11 significantly reduces clinical severity and demyelination of the spinal cord in the post-acute phase of experimental autoimmune encephalomyelitis (EAE), a mouse model for multiple sclerosis.


The Seto Lab has a long-standing interest in gene regulation and histone deacetylases (HDACs). Early on, we discovered and cloned HDAC2 and HDAC3 enzymes and performed detailed analyses of these proteins. Over the last 25 years, we have been actively studying many different aspects of histone deacetylation, including the dissection of all 18 human HDACs. Our work has led to seminal discoveries regarding regulation of histone deacetylation and identification of key non-histone targets of the HDAC enzymes. More recently, our work has extended to the analysis of how the activities/functions of histone acetyltransferases (HATs) and HDACs are interrelated, elucidating the role of HDACs in anti-tumor immunity, and identifying HDAC-specific inhibitors for disease treatments.




HDAC11 knockout mice are resistant to high-fat diet-induced obesity and metabolic syndrome, suggesting that HDAC11 functions as a crucial metabolic regulator.
Tumors after 8 and 30 weeks
Histone deacetylase 10 (HDAC10) functions as a putative tumor suppressor in mice carrying a spontaneously activated oncogenic Kras allele.