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Suming Huang

Assistant Professor
Ph.D., Mississippi State Univ., 1996
 
Research Epigenetic regulation of chromatin structure and gene expression
Office: 355 CGRC
Lab: 390B CGR
Telephone: 352-273-8199
Email: sumingh@ufl.edu

BIOGRAPHY
 
Dr. Suming Huang received his PhD in Molecular Virology from Mississippi State University in 1996. He then joined the laboratory of Dr. Stephen J. Brandt at Vanderbilt Medical Center as a postdoctoral fellow, where he worked on the transcriptional regulation of hematopoiesis. In 2001, he joined Gary Felsenfeld's group at the NIDDK/NIH to study chromatin insulator and epigenetic regulation of chromatin structure and gene expression. Dr. Huang joined the faculty at the University of Florida in 2006.
 

RESEARCH DESCRIPTION
 
Dr. Huang's lab focuses on epigenetic regulation of chromatin structure and gene expression. They study the structure and function of chromatin insulator 5’HS4, located at the 5’ end of the chicken -globin locus. The 5’HS4 possesses two kinds of insulator functions mediated by distinct proteins and cofactors. One is CTCF, which blocks inappropriate activation of a promoter by a distal enhancer, and the other acts as a chromatin barrier against encroachment of heterochromatin into adjacent euchromatin regions. The second activity relies on the binding of the transcription factors USF1/USF2 and its ability to recruit histone-modifying enzymes. Currently, they are examining the mechanisms of which USF1 maintains a local environment of active chromatin, both by biochemical and functional analysis of the USF1 containing protein complexes, and by studies of the effects of protein knockdown on the local and long-range chromatin structure and histone modification patterns. Another project for the laboratory is the regulation of TAL1 oncoprotein activity. Activation of the TAL1 gene is the most frequent gain-of-function mutation in T-cell acute lymphoblastic leukemia (TALL). They will use biochemical and epigenetic approaches to determine: 1) The mechanism underlying the ectopic activation of TAL1 transcription, 2) The mechanism dictating the TAL1 activity in normal and pathological hematopoiesis.