John J. LaPres
Associate Professor
- B.S. 1988, University of Michigan, Ann Arbor, MI
- PhD 1997, Northwestern University, Evanston, IL
- 1997-2000, Postdoctoral Researcher, University of Wisconsin, Madison, WI
lapres@msu.edu
224 Biochemistry Building
Michigan State University
East Lansing, MI 48824-1319
Office: 517-432-9282
Lab: 517-432-3269
FAX: 517-353-9334
Gene Expression supplemental data (pdf)
Hep 3B supplemental data
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John J. LaPres
Research Interests
The LaPres laboratory is focused on the PAS superfamily of transcription factors. PAS proteins (named for the first identified members, Per, ARNT and Sim) are transcription factors that play a central role in sensing and coping with changes in various environmental cues. The goal of this research is to completely understand the signaling cascades of certain PAS proteins and how they mediate their pleiotropic effects on biological systems. The work focuses on two PAS proteins in particular, the hypoxia inducible factor 1a (HIF1a) and the aryl hydrocarbon receptor (AHR) and the role they play in modulating the toxicity of metals and dioxins, respectively. The laboratory is trying to identify novel proteins and signaling cascades that might influence these two transcription factors and therefore control their ability to mediate normal biological responses and aberrant signaling leading to toxicity. In addition, the lab wants to characterize how HIF1a and the hypoxia signaling cascade influences cell cycle and cellular transformation. Hypoxia and HIF1a are critical to the development and progression of cancer and recent research from Dr. LaPres' lab and others suggest that HIF1a plays an early role in a cell's commitment to the transformed phenotype. The laboratory uses a wide range of experimental techniques, including proteomic, metabolomic and genomic technology, to gain novel insights into PAS protein signaling mechanisms and to ascertain possible mechanisms for their complex biological responses.MORE
Recent Publications
Lee K, Roth RA, Lapres JJ. Hypoxia, drug therapy and toxicity. Pharmacol Ther. 2007 Feb;113(2):229-46. Link to article.
Irwin R, Lapres JJ, Kinser S, McCabe LR. Prolyl-hydroxylase inhibition and HIF activation in osteoblasts promotes an adipocytic phenotype. J Cell Biochem. 2007 Feb 15;100(3):762-72. Link to article.
Lee K, Burgoon LD, Lamb L, Dere E, Zacharewski TR, Hogenesch JB, LaPres JJ. Identification and characterization of genes susceptible to transcriptional cross-talk between the hypoxia and dioxin signaling cascades. Chem Res Toxicol. 2006 Oct;19(10):1284-93. Erratum in: Chem Res Toxicol. 2006 Dec;19(12):1702. Link to article.
Vengellur, A., Phillips, J.M., Hogenesch, J.B. and LaPres, J.J. (2005) Gene expression profiling of hypoxia signaling in human hepatocellular carcinoma cells.
Phys. Genomics (22) 308-318. Link to pdf.
Vengellur A, LaPres JJ. (2004) The role of hypoxia inducible factor 1alpha in cobalt chloride induced cell death in mouse embryonic fibroblasts. Toxicol Sci. Dec;82(2):638-46. Epub 2004 Sep 16. Link to pdf.
Vengellur, A., Woods, B., Ryan,, H.E., Johnson, R.S. and LaPres, J.J. (2003) Gene expression profiling of the hypoxia signaling pathway in hypoxia-inducible Factor 1 a null mouse embryonic fibroblasts. Gene Expression(11) 181-197. Link to pdf.
LaPres, J. J., Glover, E., Dunham, E. E., Bunger, M. K., and Bradfield,
C. A. (2000) ARA9 modifies agonist signaling through an increase in available
aryl hydrocarbon receptor. J Biol Chem 275(9), 6153-6159. Link to pdf