Brad A. Amendt earned a Bachelor of Science in botany, a Master of Science in pathology and a Ph.D. in microbiology and molecular biology from the University of Iowa, Iowa City, Iowa. Before joining the Institute of Biosciences and Technology in 2005, Dr. Amendt held postdoctoral positions in the Departments of Biochemistry and of Physiology and Biophysics at the University of Iowa and an assistant professorship in the Department of Biological Sciences, University of Tulsa in Oklahoma. At IBT he is an associate professor in the Center for Environmental and Genetic Medicine and chairs the Graduate Student Committee.

Research Interests of Dr. Brad A. Amendt

Molecular and biochemical mechanisms of the PITX2 homeobox protein during development
Role of homeodomain genes in heart, pituitary and tooth development

Representative Publications

Brown, W.R., I. Kacskovics, B.A. Amendt, N.B. Blackmore, M. Rothschild, R. Shinde and J. E. Butler. 1995. The hinge deletion allelic variant of porcine IgA results from mutation of the splice acceptor site in the first Ca intron. J. Immunology, 154:3836-3842.

Amendt, B.A., S.S. Simpson and C.M. Stoltzfus. 1995. Inhibition of RNA splicing at the Rous sarcoma virus src 3' splice site is mediated by an interaction between a negative cis element and a chicken embryo fibroblast nuclear factor. J. Virology., 69:5068-5076.

Amendt, B.A., Z. Si and C.M. Stoltzfus, 1995. Presence of exon splicing silencers within human immunodeficiency virus type 1 tat exon 2 and tat-rev exon 3: Evidence for inhibition mediated by cellular factors. Mol. Cell. Biol., 15:4606-4615.

Si, Zhi-hai, B.A. Amendt and C.M. Stoltzfus, 1997. Splicing efficiency of human immunodeficiency virus type 1 tat RNA is determined by both a suboptimal 3' splice site and a 10 nucleotide exon splicing silencer element located within tat exon 2. Nuc. Acids Res., 25:861-867.

Zhu, Y., T. Pe'ery, J. Peng, Y. Ramanathan, N. Marshall, T. Marshall, B.A. Amendt, M. Mathews and D. Price, 1997. Transcription elongation factor P-TEFb is required for HIV-1 Tat transactivation in vitro. Genes and Dev., 11:2622