ching yi chenAssociate Professor

Research Areas
Mechanism and regulation of mammalian mRNA turnover


Dr. Ching-Yi Chen (b. 1963) is an Assistant Professor of Biochemistry and Molecular Genetics. Dr. Chen received his B.S. degree from National Cheng Kung University in Taiwan (1986) and Ph.D. degree from Baylor College of Medicine (1996). He then moved to University of California at San Diego and received his postdoctoral training in the laboratory of Dr. Michael Karin, where he was supported by three consecutive postdoctoral fellowships. He joined the faculty at UAB in 2002.

Research Interests

Post-transcriptional regulation exerted on mRNA stability is an important process in determining levels of gene expression. MRNA stability varies considerably from one mRNA species to another and is determined by specific cis-acting elements within the mRNA molecule. MRNAs encoding cytokines and proto-oncogenes are degraded rapidly in order to minimize detrimental inflammatory, immunological, or oncogenic effects. Many of these transcripts contain cis-acting instability elements within the 3’ untranslated regions that activate mRNA decay pathways. The AU-rich elements (AREs) are prominent elements that direct rapid mRNA decay by a process referred to as ARE-mediated mRNA decay (AMD). AMD is regulated by RNA-binding proteins that bind AREs and are collectively called ARE-binding proteins (ARE-BPs). Decay-promoting ARE-BPs bind ARE-containing mRNAs and target them for decay. Deregulated AMD can contribute to oncogenic transformation, inflammation, and immunopathology underlying the physiological relevance of this process. Understanding the basic mechanismsby which these unstable mRNAs are degraded is critical to reveal pathologic processes resulting from aberrant regulation of mRNA decay. Using mouse models deficient for decay-promoting ARE-BPs should also uncover the importance of AMD at the organismal level. Our research is directed to understand the mechanisms by which a decay-promoting ARE-BP, KSRP (KH-type Splicing Regulatory Protein), regulates AMD, and to investigate the in vivo functions of KSRP at the organismal level by using Ksrp knockout mice.The research in my laboratory is currently focused on the following areas: 1) understanding the role of KSRP in glucose and insulin homeostasis and 2) understanding the roles of miR-145 and miR-150 in whole-body metabolism and adipocyte functions. In addition, transcriptome-wide approaches are used to identify downstream target genes of KSRP, miR-145, and miR-150 involved in these processes. The contributions of our research are detailed understanding of how KSRP controls glucose and insulin homeostasis and how miR-145 and miR-150 control adipocyte lipid metabolism and whole-body adiposity. Our research is expected to identify novel factors governing adipocyte functions and insulin signaling that may provide future therapeutic targets to control obesity-related disorders and type 2 diabetes.


Graduate School
Ph.D., Baylor College of Medicine

Postdoctoral Fellowship
University of California, San Diego


Kaul Human Genetics Building
Room 440A
720 20th Street South
Birmingham, AL 35294-0024

(205) 934-5073