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Florida Gulf Coast University

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Dept. of Biological Sciences

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Mustafa Mujtaba

Mustafa MujtabaAssistant Professor of Microbiology
Phone: (239) 590-7357
E-Mail: mmujtaba@fgcu.edu
Office: WH 117

Education
Ph.D. in Microbiology and Cell Science, University of Florida, 1999
B.S. in Microbiology and Cell Science, University of Florida, 1995

Teaching Interests
General Chemistry I and II with Lab
Microbiology
Chemistry and Physics for Nurse Anesthetists

Research Interests
 My research interests primarily involve the study of the mechanism of interferon and cytokine function in the normal and diseased immune system and the study of normal and mutated voltage gated sodium channels in the presence of ion channel blokers. 
 Understanding the mechanism and role of cellular cytokine and humoral responses in immunological diseases may lead us to better antiviral and anti-inflammatory drugs than currently available.  For example, in the animal model of multiple sclerosis called experimental allergic encephalomyelitis, inflammatory T-helper-1 cells can be suppressed via treatment of the animal with type I interferons.  This mechanism of protection by type I interferons has been shown to be mediated via CD4 T-helper-2 cells and CD4 T-regulatory cells that secrete cytokines such as interleukin-10 and tumor growth factor beta (TGF-b), which act synergistically to inhibit the inflammatory T cell that cause the debilitating autoimmune disease in the animal.  Thus, by suppressing or enhancing specific cellular and humoral responses of the immune system, we may be better able to alleviate and or prevent immunological diseases, such as multiple sclerosis.
My other long-term objective is to better understand how normal and mutated voltage-gated sodium channels function in the presence of ion-channel blockers.   Regions of the voltage gated sodium channel other than the traditional local anesthetic receptor sites can be targeted to enhance the drug design, duration, and or differential effect of the local anesthetic and to improve therapeutics for sodium channel-associated pathologies such as cardiac arrhythmias and cardiac deaths related to the LQT-3 form of the long QT syndrome.

Selected Publications
1. Mujtaba MG, Soos JM, Johnson HM.  CD T suppressor cells mediate interferon tau protection against experimental allergic encephalomyelitis.  Journal of Neuroimmunology 1997; 75:35-42.
2. Mujtaba MG, Streit WJ, Johnson HM.  IFN-? suppresses both the autoreactive humoral and cellular immune responses and induces stable remission in mice with chronic experimental allergic encephalomyelitis.  Cellular immunology 1998; 186:94-102.
3. Mujtaba MG and Johnson HM.  IFN? inhibits IgE production in a murine model of allergy and in a IgE-producing human myeloma cell line.  The Journal of Allergy and Clinical Immunology 1999; 104(5):1037-1044.
4. Gerner PG, Mujtaba MG, Sinnott CJ, and Wang GK.  Amitriptyline versus bupivacaine in rat sciatic nerve blockade.  Anesthesiology 2001; 94(4):661-667.
5. Mujtaba MG, Gerner PG, and Wang GK.  Local anesthetic properties of prenylamine.  Anesthesiology 2001; 95:1198-1204.
6. Mujtaba MG, Wang S-Y, and Wang GK.  Prenylamine block of Nav1.5 channel is mediated via a receptor distict from that of local anesthetics. Molecular Pharmacology 2002; 62(2):415-22.
7. Gerner PG, Mujtaba MG, Khan M, Sudoh Y, Vlassakov K, Anthony DC, and Wang GK. N-Phenylethyl Amitriptyline in Rat Sciatic Nerve Blockade. Anesthesiology 2002; 96(6):1435-42.
8. Gerner P, Haderer AE, Mujtaba MG, Sudoh Y, Narang S, Abdi S, Srinivasa V, Pertl C, Kuo Wang G.  Assessment of Differential Blockade by Amitriptyline and Its N-Methyl Derivative in Different Species by Different Routes.  Anesthesiology  2003 98(6):1484-1490.
9. Flowers LO, Johnson HM, Mujtaba MG, Ellis MR, Haider SMI, and Subramaniam PS. (2004)  Characterization of a peptide inhibitor of JAK2 that mimics SOCS-1 function. J. Immunology.  15;172(12):7510-8.
10. Mujtaba MG, Flowers L, Patel C, Patel R, Haider M, and Johnson HM.  Treatment of mice with the Supressor of cytokine signaling peptide 1, Tyrosine kinase inhibitor peptide, prevents development of the acute form of experimental allergic encephalomyelitis and induces stable remission in the chronic relapsing/remitting form.  Journal of Immunology 2005, 175:5077-5068.
11. Mujtaba MG, Patel CB, Patel RA, Flowers LO, Burkhart MA, Waiboci LW, Martin J, Haider MI, Ahmed CM, Johnson HM.  The gamma interferon (IFN-?) mimetic peptide IFN-gamma (95-133) prevents encephalomyocarditis virus infection both in tissue culture and in mice.  Clin. Vaccine Immunol. 2006, 13(8):944-52.

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