Suming Huang, Ph.D.


Research: Epigenetic regulation of chromatin structure and gene expression

Ph.D. from Mississippi State Univ., 1996


Contact Information:
     Office: 355 CGRC
     Lab: 390B CGRC
     Telephone: (352) 273-8199


Dr. Suming Huang received his PhD in Molecular Virology from Mississippi State University in 1996. He then joined Dr. Stephen Brandt’s laboratory 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 NIDDK/NIH to study the chromatin insulator and epigenetic regulation of chromatin structure and gene expression.  Dr. Huang joined the faculty at the University of Florida in 2006.


Epigenetic modifications play an important role in chromatin organization and gene expression.  Perturbation of this process often leads to cancer.  My lab is interested in understanding the epigenetic mechanism that underlies the controls of the enhancer and promoter interaction during transcriptional activation. We are currently focusing on examining the epigenetic mechanisms by which the chromatin insulator binding factor USF1 maintains a local environment of active chromatin, both by biochemical and functional analysis of the USF1 associated histone modifying enzyme complexes. We are also studying the effects of these complexes on histone modification patterns, local and long-range chromatin structure, and transcriptional regulation.

Another project that my lab is focusing on is the transcriptional regulation of TAL1/SCL, which plays a critical role in normal and malignant hematopoiesis. Activation of TAL1 is the most frequent gain-of-function mutation occurring in T-cell lymphoblastic leukemia (T-ALL). We will use biochemical and cell biology approaches such as protein purification, siRNA knockdown, tissue culture, ChIP-Seq, ChIP, microarray, and in vitro and in vivo transformation assays to determine: 1) the mechanism that triggers the ectopic activation of TAL1 transcription in T-ALL, and 2) the mechanism that dictates the TAL1 transcriptional activity in normal and malignant hematopoiesis.