Department of Biology and Biochemistry
Office: HSC 402C
Contact: email@example.com - (713) 743-8374
Education: Ph.D., Harvard University
My research laboratory group is interested in the mechanisms of signal transduction, especially in the nervous system. A major aim of our research is to understand the role of altered signal transduction in the development of abnormal nerve function in diabetes. Cell signaling is being studied in peripheral nerve from normal and experimentally diabetic rats. We have documented biochemical abnormalities in diabetic nerve that affect inositol phospholipid turnover, diacylglycerol levels, arachidonic acid metabolism and protein phosphorylation. A second, complementary, approach utilizes cultured Schwann cells grown under conditions intended to mimic the diabetic condition, such as an elevated medium glucose level.
Recently, we have initiated investigations of signal transduction and lipid metabolism defects in ataxia telangiectasia (A-T), a rare human autosomal recessive disease which affects both the nervous and immune systems. The mutated gene codes for a protein (ATM) which is involved in both nuclear and cytoplasmic functions. In these studies, signaling and lipid metabolic patterns are being investigated in subcellular fractions and during cell cycle progression, using cultured human fibroblasts obtained from normal individuals and AT patients.
A third area of interest is to elucidate the function of serine and tyrosine phosphate groups present in P0, the major peripheral myelin protein. Phosphorylation of this cell adhesion molecule is greatest during the period of active myelination, suggesting a key role for this post-translational modification in myelin assembly and maturation. The approach we are taking is to transfect cultured cells with the normal or mutated gene for P0 and to study the distribution of the expressed wild type and mutant protein within the cell, the extent of P0 phosphorlyation and effects on cellular properties.
- Konde V, Eichberg J. (2006). Myelin protein zero: mutations in the cytoplasmic domain interfere with its cellular trafficking. Journal of Neuroscience Research, 83(6):957-64.
- Eichberg J. (2002). Myelin P0: new knowledge and new roles. Neurochemical Research, 27(11):1331-40.
- Eichberg J. (2002). Protein kinase C changes in diabetes: is the concept relevant to neuropathy? International review of Neurobiolgy, 50:61-82.
- Mîinea C, Kuruvilla R, Merrikh H, Eichberg J. (2002). Altered arachidonic acid biosynthesis and antioxidant protection mechanisms in Schwann cells grown in elevated glucose. Journal of Neurochemistry, 81(6):1253-62.
- Yorek, M., Dunlap, J.A., Manzo-Fontes, A., Bianchi, R., Berry, G. and Eichberg, J. 1999 Abnormal myo-Inositol and Phospholipid Metabolism in Cultured Fibroblasts from Patients wth Ataxia-Telangiectasia. Biochim. Biophys. Acta 1437, 287-300.
- Kuruvilla, R. and Eichberg, J. 1998 Depletion of Phospholipid Arachidonoyl-Containing Species in a Human Schwann Cell Line Grown in Elevated Glucose and their Restoration by an Aldose Reductase Inhibitor. J. Neurochem. 71: 775-783
- Kuruvilla, R., Peterson, R.G., Kincaid, J.C. and Eichberg, J. 1998 Evening Primrose Oil Treatment Corrects Reduced Conduction Velocity but not Depletion of Arachidonic Acid in Nerve from Streptozotocin-Induced Diabetic Rats. Prostaglandins, Leukotrienes
- Mathew, J., Bianchi, R., McLean, W.G., Peterson, R.G., Roberts, R.E., Saravesi, S. and Eichberg, J. 1997. Phosphoinositide Metabolism, Na,K-ATPase and Protein Kinase C are Altered in Peripheral Nerve from Zucker Fatty Diabetic Rats (ZDF/Gmi-Fa). Neurosci.