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Naren Banik, Ph.D.
Medical University of South Carolina, Charleston, SC Phone: (843) 792-3946 Education:
Research Interests: These studies are continuing in experimental animal models. I have localized calpain in myelin by biochemical and immunocytochemical methods and examined how it may be regulated. I am currently studying the source of this enzyme in CNS injury, demyelinating diseases, and optic nerve degeneration in glaucoma and have taken cellular and molecular approaches to study its expression both at the gene and protein levels. My laboratory is also exploring the role of calpain in apoptotic cell death mechanisms in CNS. Findings of its increased activity and content in CNS trauma led me to examine whether (1) calpain stimulation and expression is regulated by cytokines (or other factors) and (2) use of calpain-specific inhibitors as therapeutic agents in spinal cord injury and in close animal models of MS will be neuroprotective. Selected Recent Publications: Deshpande RV, Goust JM, Chakrabarti AK, Barbosa E, Hogan EL, Banik NL. Calpain expression in lymphoid cells: Increased mRNA and protein levels after cell activation. J Biol Chem 1995: 270(6):2497-2505. Li Z, Banik NL. The localization of mcalpain in myelin: Immunocytochemical evidence in different areas of rat brain and nerves. Brain Res 1995:697:112-121. Banik NL, Matzelle D, Gantt-Wilford G, Hogan EL. Increased calpain content and progressive degradation of neurofilament protein in spinal cord injury. Brain Res 1997:752:301-306. Banik NL, Matzelle DC, Terry EC, Hogan EL. A new mechanism of methylprednisolone and other corticosteroids action demonstrated in vitro: Inhibition of a proteinase (calpain) prevents myelin and cytoskeletal protein degradation. Brain Res 1997:748:205-210. Shields DC, Tyor WR, Deibler GE, Hogan EL, Banik NL. Increased calpain expression in activated glial and inflammatory cells in experimental allergic encephalomyelitis. Proc Natl Acad Sci, USA 1998: 95:5768-5772.
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