詹明修（Ming-Shiou Jan）

中山醫學大學微生物免疫學科助理教授

Assistant Professor, 2000 - 2002, Department of Pharmacy, Chia Nan University of Pharmacy and Science.

Ph.D., 2000, Medical College, National Cheng Kung University.

msjan@csmu.edu.tw
Office: 04-24730022 ext. 11632
Lab: 04-24730022 ext. 11633
FAX: 04-24727178

Representative Publications

Lin, Y. S., S. C. Hu, M. S. Jan, and T. J. Rogers. 1991. Inhibition of the delayed-type hypersensitivity response by staphylococcal enterotoxin B-induced suppressor T cells. Cell. Immunol. 132:532-538.

Lin, Y. S., H. Y. Lei, T. L. Low, C. L. Shen, L. J. Chou, and M. S. Jan. 1992. In vivo induction of apoptosis in immature thymocytes by staphylococcal enterotoxin B. J. Immunol. 149:1156-1163.

Lin, Y. S., M. S. Jan, and H. I. Chen. 1993. The effect of chronic and acute exercise on immunity in rats. Int. J. Sports Med. 14:86-92.

Lin, Y. S., M. S. Jan, T. J. Tsai, and H. I. Chen. 1995. Immunomodulatory effects of acute exercise bout in sedentary and trained rats. Med. Sci. Sports Exerc. 27:73-78.

Lin, Y. S., S. F. Kao, M. S. Jan, M. L. Cheng, L. Y. C. Wing, W. C. Chang, H. Y. Lei, and M. T. Lin. 1995. Changes of protein kinase C subspecies in staphylococcal enterotoxin-B-induced thymocyte apoptosis. Biochem. Biophys. Res. Commun. 213:1132-1139.

Chang, M. Y., M. S. Jan, S. J. Won, and H. S. Liu. 1998. Ha-rasVal12 oncogene increases susceptibility of NIH/3T3 cells to lovastatin. Biochem. Biophys. Res. Commun. 248:62-68.

Lin, Y. S., Y. T. Huang, P. S. Chen, C. F. Lin, M. S. Jan, and H. Y. Lei. 1999. Requirement of I-E molecule for thymocyte apoptosis induced by staphylococcal enterotoxin B in vivo. Cell. Immunol. 193:71-79.

Chang, M. Y., S. J. Won, B. C. Yang, M. S. Jan, and H. S. Liu. 1999. Selective activation of Ha-ras val12 oncogene increases susceptibility of NIH/3T3 cells to TNF-alpha. Exp. Cell Res. 248:589-598.

Liu, H. S., M. S. Jan, C. K. Chou, P. H. Chen, and N. J. Ke. 1999. Is green fluorescent protein toxic to the living cells? Biochem. Biophys. Res. Commun. 260:712-717.

Jan, M. S., L. Y. C. Wing, M. T. Lin, and Y. S. Lin. 1999. a-Difluoromethylornithine blocks thymocyte apoptosis via reduction of tyrosine phosphorylation. Scand. J. Immunol. 50:605-611.

Jan, M. S., H. S. Liu, and Y. S. Lin. 1999. Bad overexpression sensitizes NIH/3T3 cells to undergo apoptosis which involves caspase activation and ERK inactivation. Biochem. Biophys. Res. Commun. 264:724-729.

Hsu, L. J., M. S. Jan, and Y. S. Lin. In vivo staphylococcal enterotoxin B (SEB)-primed murine splenocytes secrete mediators which suppress CD25hi expression and cell cycle progression of naive splenocytes in response to SEB in vitro. Cell. Immunol. 201(1):50-57.

Lee, P. C., C. J. Hung, H. Y. Lei, T. T. Chang, J. R. Wang and M. S. Jan. 2000. Parvovirus B19-related acute hepatitis in an immunosuppressed kidney transplant. Nephrol. Dial. Transpl. 15:1486-488.

Lee, P.C., C. J. Hung, Y. J. Lin, J. R. Wang, M. S. Jan, and H. Y. Lei. 2002. A role for chronic parvovirus B19 infection in liver dysfunction in renal transplant recipients? Transplantation. 73(10):1635-1639.

Kuo, J-H S., M. S. Jan. and K. C. Sung. 2003. Evaluation of the stability of polymer-based plasmid DNA delivery systems after ultrasound exposure. International Journal of Pharmaceutics. 257:75-84.

Lin CF, Chen CL, Chang WT, Jan MS, Hsu LJ, Wu RH, Tang MJ, Chang WC, Lin YS. Sequential caspase-2 and caspase-8 activation upstream of mitochondria during ceramide- and etoposide-induced apoptosis. J Biol Chem. 2004 Sep 24;279(39):40755-61. Epub 2004 Jul 15

相關研究計畫

NSC 93-2320-B-040-009-
Roles of the novel tumor suppressor Wox1 on apoptotic signaling (2/3)
新腫瘤抑制基因WOX1在凋亡途徑所扮演的角色(2/3)
PI

The goal of this research is to study the role of Wox expression profiles on tumor metastasis. In addition, the protein modification, translocation, and interaction with other proteins is still going.

NSC 92-2320-B-040-052-
Roles of the novel tumor suppressor Wox1 on apoptotic signaling (1/3)
新腫瘤抑制基因WOX1在凋亡途徑所扮演的角色(1/3)
PI

The goal of this research is to study the role of Wox1 in ceramide-induced immune cell death. Previous results showed that treatment of 10I T hybridoma cells with lithium inhibited apoptotic death induced by ceramide. Further investigation revealed that Wox1 expression profiles of apoptotic cells different from survival cells. Lithium treatment reverse ceramide-mediated Wox1 expression. We propose the changes may be regulated by posttranslational modification such as sumoylation. On the other hand, Wox1 translocation in ceramide-induced apoptotic system also be investigated.

NSC 91-2320-B-040-052-
Study on apoptotic signal pathways and survival pathways: roles of Hsp70 and Wox1 on ceramide induced apoptosis
細胞凋亡訊息與存活訊息途徑的探討:Hsp70與WOX1在抑制ceramide誘導之細胞凋亡機制中所扮演的角色

The goal of this research is to study the role of lithium, which has been shown to confer protection against neuronal apoptosis, in ceramide-induced immune cell death. Previous results showed that treatment of 10I T hybridoma cells with lithium inhibited apoptotic death induced by ceramide. Further investigation revealed that lithium augmented MEK and ERK phosphorylation. The MEK inhibitor PD98059 reduced lithium-induced MEK/ERK activation and cell survival. In search for the downstream target of ERK, studies indicated that lithium enhanced Hsp70 expression and Hsp inhibitor moderately abolished lithium-mediated protection of ceramide-induced apoptosis. These results indicated that lithium stimulated a survival pathway that involved activation of MEK, ERK and Hsp70.