Chuenchanok
Khodthong
E-mail:cfrasier@wisc.edu
Research Project:
Ca2+-dependent vesicle exocytosis is a cellular mechanism for secretion that is essential for communication in the nervous and endocrine systems. Two types of secretory vesicles have been identified. Synaptic vesicles (SVs) contain neurotransmitters for release into synaptic clefts from the presynaptic active zone of nerve terminals to mediate intercellular communication. Dense core vesicles (DCVs) store and release biogenic amine neurotransmitters, neuropeptides, and hormones from neuroendocrine and endocrine cells to support a wide variety of biological processes.
Ca2+-dependent activator protein for secretion (CAPS) is a neuronal/endocrine specific protein that functions selectively in Ca2+-dependent DCV exocytosis, but not SV exocytosis. It has been shown to interact with phosphatidylinositol 4,5-bisphosphate and syntaxin1A on the plasma membrane, however the functional relevance of these interactions remains unclear. My work in the Martin lab will be to test the hypothesis that CAPS utilizes its syntaxin and PIP2 binding properties to organize PIP2 and syntaxin clusters in the plasma membrane, consequently establishing fusion sites for DCV exocytosis.
Abstracts and Publications:
- Brautigam, V.M., C. Frasier, M. Nikodemova, and J.J. Watters. 2005. Purinergic receptor modulation of BV-2 microglial cell activity: Potential involvement of p38 MAP kinase and CREB. J. Neuroimmunol. 66:113-125. [PDF]
- Frasier, C. and J.J.Watters. 2004. Potential role for p38 MAP kinase and CREB in mediating adenine nucleotide inhibition of nitric oxide production in BV-2 murine microglial cells. Soc. Neurosci. Abstr.
- Frasier, C. and J.J. Watters. 2003. Purinergic receptor modulation of nitric oxide production in the mouse microglial cell line, BV-2. Soc. Neurosci. Abstr.