MARY K. DAHMER
ASSISTANT PROFESSOR
EDUCATION:
B.S. 1977, The University of Michigan, Ann Arbor, Michigan
Ph.D. 1983, The University of Michigan, Ann Arbor, Michigan
Postdoctoral Fellow: 1983-84, The University of Michigan, Ann Arbor, Michigan;
1984-90, The University of Illinois at Chicago and the University of Chicago
RESEARCH INTERESTS: My research has focused on understanding the
mechanisms by which hormones, growth factors and neurotransmitters regulate
cellular functions. Many of these agents act via second messengers such
as cAMP, Ca2+, diacylglycerol and phosphoinositides. My particular interests
lie in identifying and studying agents which affect the survival or the
differentiated functions of neuronal cells. Recent work in my laboratory
is aimed at understanding how insulin-like growth factor-I (IGF-I) affects
cells of the nervous system. IGF-I is synthesized by many types of cells
and appears to act as an autocrine or paracrine growth factor. IGF-I belongs
to the class of polypeptides which binds to membrane receptors with intrinsic
tyrosine kinase activity. We have found that IGF-I stimulates proliferation
of PC12 pheochromocytoma cells and enhances secretagogue-stimulated catecholamine
synthesis and secretion in normal chromaffin cells. Catecholamine synthesis
and secretion in chromaffin cells is triggered by a rise in intracellular
free Ca2+, primarily due to influx of Ca2+ via voltage-dependent Ca2+ channels.
Recent work in my laboratory suggests that protein kinase C (Ca2+, phospholipid
dependent protein kinase) is required for the enhanced secretion caused
by IGF-I. Another project in the laboratory is aimed at understanding the
mechanism by which dopamine agonists acutely inhibit catecholamine secretion.
CURRENT RESEARCH SUPPORT:
"Mechanism of Insulin-Like Growth Factor-I Effects on Chromaffin Cell
Function; October 1, 1992 - September 30, 1997; $350,000 TDC.
PUBLICATIONS:
1. Leach, K.L., Dahmer, M.K., Hammond, N.D., Sando, J.J. and Pratt, W.B.
(1979) Molybdate inhibition of glucocorticoid receptor inactivation and
transformation. J. Biol. Chem., 254, 11884-11890.
2. Dahmer, M.K., Quasney, M.W., Bissen, S.T., and Pratt, W.B. (1981) Molybdate
permits resolution of untransformed glucocorticoid receptors from the transformed
state. J. Biol. Chem., 256, 9401-9495.
3. England, B.G., Dahmer, M.K., and Webb, R. (1981) Relationships between
follicular size and antral fluid steroid concentrations at three stages
of the estrous cycle in the ewe. Biol. Reprod., 24, 1068-1075.
4. England, B.G., Webb, R., and Dahmer, M.K. (1981) Follicular steroidogenesis
and gonado-tropin binding to ovine follicles during the estrous cycle.
Endocrinology, 109, 881-887.
5. Leach, K.L., Housley, P.R., Grippo, J.F., Dahmer, M.K., and Pratt, W.B.
(1982) Characteristics of a glucocorticoid receptor stabilizing factor.
J. Biol. Chem., 257, 381-388.
6. Housley, P.R., Dahmer, M.K. and Pratt, W.B. (1982) Inactivation of glucocorticoid
binding capacity by protein phosphatases in the presence of molybdate and
complete reactivation by dithiothreitol. J. Biol. Chem., 257, 8615-8618.
7. Leach, K.L., Dahmer, M.K. and Pratt, W.B. (1983) Unexpected effects
of molybdate on glucocorticoid receptors. J. Steroid Biochem., 18,
105-107.
8. Grippo, J.F., Tienrungroj, W., Dahmer, M.K., Housley, P.R., and Pratt,
W.B. (1983) Evidence that the endogenous heat stable glucocorticoid receptor
activating factor is thioredoxin.
J. Biol. Chem., 258, 13658-13664.
9. Dahmer, M.K., Housley, P.R. and Pratt, W.B. (1984) Effects of molybdate
and endogenous inhibitors on steroid receptor inactivation, transformation,
and translocation. Ann. Rev. Physiol., 46, 67-81.
10. Housley, P.R., Grippo, J.F., Dahmer, M.K., and Pratt, W.B. (1984) Inactivation,
activation and stabilization of glucocorticoid receptors. In G. Litwack
(Ed.), Biochemical Actions of Hormones, Vol. 11 (pp. 347-376). New
York: Academic Press.
11. Pratt, W.B., Housley, P.R., Dahmer, M.K., and Grippo, J.F. (1984) Phosphorylation
of the glucocorticoid receptor. In W. Paton, J. Mitchell and P. Turner
(Eds.), IUPHAR Ninth International Congress of Pharmacology (pp.
93-99). London: MacMillan Press.
12. Dahmer, M.K., Tienrungroj, W., and Pratt, W.B. (1985) Purification
and preliminary characterization of a macromolecular inhibitor of glucocorticoid
receptor binding to DNA.
J. Biol. Chem., 260, 7705-7715.
13. Dahmer, M.K. and Perlman, R.L. (1988) Insulin and insulin-like growth
factors stimulate deoxyribonucleic acid synthesis in PC12 pheochromocytoma
cells. Endocrinology, 122, 2109-2113.
14. Dahmer, M.K. and Perlman, R.L. (1988) Bovine chromaffin cells have
IGF-I receptors: IGF-I enhances catecholamine secretion. J. Neurochem.,
51, 321-323.
15. Dahmer, M.K., Ji, L., and Perlman, R.L. (1989) Characterization of
insulin-like growth factor-I receptors in PC12 pheochromocytoma cells and
bovine adrenal medulla. J. Neurochem., 53, 1036-1042.
16. Dahmer, M.K. and Perlman, R.P. (1989) Effects of insulin-like growth
factor-I on chromaffin cells. In M. Raizada and D. LeRoith (Eds.), Molecular
and Cellular Aspects of Insulin, Insulin-like Growth Factors and Their Receptors:
Implications for the Central Nervous System (pp. 467-472). New York:
Plenum Press.
17. Dahmer, M.K., Hart, P.M., and Perlman, R.L. (1990) Studies on the effect
of insulin-like growth factor-I on catecholamine secretion from chromaffin
cells. J. Neurochem., 54, 931-936.
18. Artalejo, C.R., Dahmer, M.K., Perlman, R.L., and Fox, A.P. (1991) Two
types of Ca currents are found in bovine chromaffin cells: Facilitation
is due to the recruitment of one type. J. Physiol. (London), 432,
681-707.
19. Dahmer, M.K., Hart, P.M., and Perlman, R.L. (1991) Insulin-like growth
factor-I enhances tyrosine hydroxylase activation in bovine chromaffin cells.
J. Neurochem., 57, 1347-1353.
20. Penberthy, W.T. and Dahmer, M.K. (1994) Insulin-like growth factor-I
enhanced secretion is abolished in protein kinase C-deficient chromaffin
cells. J. Neurochem., 62, 1707-1715.
21. Dahmer, M.K. (1995) Down-regulation of protein kinase C activity preferentially
attenuates high K+ stimulated tyrosine hydroxylase activity in adrenal chromaffin
cells cultured with insulin-like growth factor-I. Neurosci. Lett.,
in press.
22. Dahmer, M.K. and Senogles, S.E. (1996) Dopaminergic inhibition of catecholamine
secretion from chromaffin cells: Evidence that inhibition is mediated by
D4 and D5 dopamine receptors.
J. Neurochem., 66, in press.