Frank Rozsa

Frank Rozsa, PhD

Research Investigator

Phone: (734) 764-0059

Fax: (734) 647 0228

Research Interests

I am currently utilizing microarray technology to examine the expression of thousands of genes in cultured human trabecular meshwork (HTM) cells. Since HTM is responsible for the outflow of aqueous in the eye, changes in gene expression that can alter the ability of this tissue to mediate outflow need to be examined. Microarrays are a powerful tool that gives the investigator the ability to scan thousands of genes for changes in expression, especially when used in conjunction with techniques such as real-time PCR to validate the findings. Comparison of gene expression changes in normal HTM cells treated with glucocorticoids that increase the expression of myocilin (a known glaucoma gene) to age and sex-matched glaucomatous HTM will provide a method of mapping the biochemical pathway for myocilin. We also plan to explore changes in gene expression in normal tissue treated with inhibitors of protein synthesis, elevated glucose, and an anti-inflammatory drug, diclofenac.

Education

1991 - 1996 Postdoctoral Research Fellow, Department of Microbiology, Biozentrum, University of Basel, Switzerland, Laboratory of Werner Arber, PhD.
1988 - 1991 University of Michigan, Ann Arbor, Michigan. PhD in Epidemiologic Sciences; Advisor: Carl F. Marrs, PhD.
1986 - 1988 University of Michigan, Ann Arbor, Michigan. Master of Public Health in Hospital and Molecular Epidemiology.
1980 - 1984 University of Michigan, Ann Arbor, Michigan. Bachelor of Science in Cell and Molecular Biology.

Publications

Shimizu S, Lichter PR, Johnson AT, Zhou Z, Higashi M, Gottfredsdottir M, Othman M, Moroi SE, Rozsa FW, Schertzer RM, Clarke MS, Schwartz AL, Downs CA, Vollrath D, and Richards JE. Age-dependent prevalence of mutations at the GLC1A Locus in Primary Open-angle Glaucoma. Am J Ophthal 2000; 130:165-177.
Zimmerman CC, Lingappa VR, Richards JE, Rozsa FW, Lichter PR, and Polansky JR. A trabecular meshwork glucocorticoid response (TIGR) gene mutation affects translocational processing. Mol Vis. 1999 Aug 23;5:19
Rozsa FW, Shimizu S, Lichter PR, Johnson AT, Othman MI, Scott K, Downs CA, Nguyen TD, Polansky J and Richards JE. (1998) GLC1A mutations point to regions of potential functional importance on the TIGR/MYOC protein (PDF). Molecular Vision 4:20 .
Richards JE, Ritch R, Lichter PR, Rozsa FW, Stringham HM, Caronia RM, Johnson D, Abundo GP, Willcockson J, Downs CA, Thompson DA, Musarella MA, Gupta N, Othman MI, Torrez DM, Herman SB, Wong DJ, Higashi M, Boehnke M. (1998) Novel trabecular meshwork inducible glucocorticoid response mutation in an eight-generation juvenile-onset primary open-angle glaucoma pedigree. Ophthalmology 105:1698-1707.
Rozsa FW, Meyer TF, and Fussenegger M. (1997) Inversion of Moraxella lacunata type 4 pilin genes sequences by a Neisseria gonorrhoeae site-specific recombinase. J Bacteriol 179:2382-2388.
Rozsa FW, Viollier P, Fussenegger M, Hiestand-Nauer R, and Arber W. (1995) Cin-mediated recombination at secondary crossover sites on the Escherichia coli chromosome. J Bacteriol 177:1159-1168.
Tonjum T, Marrs CF, Rozsa FW, and Bovre K. (1991) The type 4 pilin of Moraxella nonliquefaciens exhibits unique similarities with the pilins of Neisseria gonorrhoeae and Dichelobacter nodosus. J Gen Microbiol 137:2483-2490.
Rozsa FW and Marrs CF. (1991) Interesting sequence differences between the pilin gene inversion regions of Moraxella lacunata ATCC17956 and Moraxella bovis Epp63. J Bacteriol 173:4000-4006.
Marrs CF, Rozsa FW, Hackel MA, Stevens SP, and Glasgow AC. (1990) Identification, cloning and sequencing of piv, a new gene involved in inverting the pilin genes of Moraxella lacunata. J Bacteriol 172:4370-4377.
Foster CM, Shafer JA, Rozsa FW, Wang X, Lewis SD, Renken DA, Natale JE, Schwartz J, and Carter-Su C. (1988) Growth Hormone promoted tyrosyl phosphorylation of Growth Hormone receptors in murine 3T3-F442A fibroblasts and adipocytes. Biochemistry 27:326-334.
Carter-Su C, Rozsa FW, Wang X, and Stubbart JR. (1988) Rapid and transitory stimulation of 3-o-methylglucose transport by Growth Hormone. Am J Physiol 255:723-729.

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