Professor

Department of Molecular and Cellular Biochemistry
and Center for Molecular Neurobiology

Ph.D.: Massachusetts Institute of Technology
Postdoctoral Fellow: Harvard University

Center for Molecular Neurobiology
The Ohio State University
174 Rightmire Hall
1060 Carmack Road
Columbus, OH 43210

Phone: 614-292-2910
Fax: 614-292-5379
E-mail: Hai.2@osu.edu

Link to NLM & NIH PubMed publications list for Tsonwin Hai (last 10 years)

Review articles/book chapters:
Review_1999.pdf
Review_2001.pdf
Review_Chpt_20_2006.pdf
ATF_Hai_T.pdf

• Eukaryotic gene expression
• Stress response
• Cell death (apoptosis)
• Cell cycle regulation
• Signal transduction
• Molecular mechanisms of diseases including cancer and diabetes

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Research Description:

Cancer and many diseases are manifestations of over expression or under expression of a gene or a group of genes. Although there are many regulatory steps in the process of gene expression, many lines of evidence indicate that transcriptional control is the focal point of regulation. My laboratory is investigating the transcriptional regulation in eukaryotes. Specifically, we are investigating the mammalian ATF/CREB family of transcription factors. Previously, we demonstrated that a specific member of this family, ATF3, is induced by a variety of physiological stresses: heart attack, liver injury, kidney injury, skin wounding and seizures. Interestingly, transgenic mice expressing ATF3 in various tissues exhibit defects in the corresponding tissues: mice expressing ATF3 in the heart have conduction abnormalities and contractile dysfunction; mice expressing ATF3 in the liver have liver dysfunction and defect in gluconeogenesis; mice expressing ATF3 in the ductal epithelium have defect in endocrine pancreas development and beta cell deficiency. We are taking three directions to follow up on these observations:

1. We are investigating the signal transduction pathways for the induction of ATF3 by stress signals.
2. We are further investigating the physiological functions of ATF3 by the gain-of-function and loss-of-function approaches. For gain-of-function approach, we are using the mifepristone (MFP)-inducible system to generate transgenic mice expressing ATF3 in specific tissues to investigate the molecular mechanisms by which it induces dysfunction in the corresponding tissues. We are also expressing ATF3 in cultured cells by adenoviral and lentiviral targeting methods to investigate the roles of ATF3 in cell cycle regulation and apoptosis. For loss-of-function approaches, we are analyzing knock-out mice deficient in ATF3. In addition, we are Òknocking-downÓ ATF3 in cultured cells by RNAi to investigate its roles in various cellular functions.
3. We are investigating the roles of ATF3 in the pathogenesis of several stress-associated diseases, particularly diabetes, cancer and liver dysfunction.

Therefore, our studies of eukaryotic gene expression have led us to the investigation of stress responses, signal transduction, apoptosis, cell cycle regulation, and disease models.

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Techniques and Models:

• Molecular biology
• Cell biology
• Biochemistry
• Genetics and physiology
• Microarray, proteomics, and bioinformatics