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中山醫 生醫系
蕭光明

 

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蕭光明 教授

 

 

(Dr. Kuang-Ming Hsiao)

 

 

 

中正大學生命科學系

 

 

 

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Tel:(05)2720411 ext 66512

 

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 學歷:

 1995 博士 美國威斯康辛大學麥迪森分校 癌症生物實驗室

 1987 碩士 陽明醫學院 生物化學研究所

 1985 學士 台灣大學 農業化學系

 

 經歷:

 2008 ~ present 教授 中正大學 生命科學系

 2003 ~ 2008 教授 中山醫學大學 生物醫學科學學系 

 1997 ~ 2003 副教授 中山醫學大學 生命科學系

 1995 ~ 1997 博士後研究員 美國北卡大學教堂山校區

 

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  • 腫瘤生物學

 

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A. 期刊論文

1.  Lin M.-J., Huang R.-Y., Pan H., and Hsiao K.-M.* (2008) Functional studies of the effect of NO donor on human CLCN1 polymorphism/ mutants expressed in Xenopus laevis oocytes. Biochem Biophys Res Commun. 365(4): 724-728. (SCI)

2.  Wang L.-C., Hung W.-T., Pan H*., Chen K.-Y., Wu Y.-C., Liu Y.-F., and Hsiao K.-M.* (2008) Growth-dependent effect of muscleblind knockdown on Caenorhabditis elegans. Biochem Biophys Res Commun. 366 (3): 705-709. (SCI)

3.  Chang TY, Kuo HC, Hsiao K-M, Huang CC. (2007) Phenotypic Variability of Autosomal Dominant Myotonia Congenita in aTaiwanese Family with Muscle Chloride Channel (CLCN1) Mutation. J Acta Neurol. Taiwanica 2007; 16(4):214-220

4.  Chen KY, Pan H, Lin MJ, Li YY, Wang LC, Wu YC, and Hsiao K.-M.*. (2007) Length-dependent toxicity of untranslated CUG repeats on Caenorhabditis elegans. Biochem Biophys Res Commun. 352(3):774-779. (SCI)

5.  Lin M.-J., You T.-H., Pan H., and Hsiao K.-M.* (2006) Functional characterization of CLCN1mutations in Taiwanese patients with myotonia congenita via heterologous expression. Biochem Biophys Res Commun. 351(4): 1043-1047.(SCI)

6.  K uo H.-C., Hsiao K.-M., Chang L.-I., You T.-H., Yeh T.-H., and Huang C.-C*. (2006) Novel mutations at carboxyl terminus of CIC-1 channel in myotonia congenita. Acta Neurol Scand. 113: 342–346. (SCI)

7.  Kuo H.-C., Huang C.-C.*, Chu C.-C., Wai Y.-Y., Hsiao K.-M., and Chu N.-S. (2006) Congenital myotonic dystrophy: variability in muscle involvement and histopathological process. J Acta Neurol. Taiwanica 15(1): 13-20.

8.  K uo H.-C., Hsiao K.-M., Chen C.-J., Hsieh Y.-C., and Huang CC.* (2005) Brain magnetic resonance image changes in a family with congenital and classic myotonic dystrophy. Brain Dev. 27(4):291-296. (SCI)

9.  L i Y.-C., Cheng Y.-M., Hsieh L.-J., Ryder O.-A., Yang F., Liao S.-J., Hsiao K.-M., Tsai F.-J., Tsai C.-H., and Lin C.-C.* (2005) Karyotypic evolution of a novel cervid satellite DNA family isolated by microdissection from the Indian muntjac Y-chromosome. Chromosoma 114(1):28-38. (SCI)

10. J ou S.-B., Chang L.-I., Pan H., Chen P.-R., and Hsiao K.-M.* (2004) Novel CLCN-1 mutations in Taiwanese patients with myotonia congenita. Journal of Neurology 251: 666-670. (SCI)

11. K uo H.-C., Huang C.-C.*, Chu C.-C., Chiang S.-Y., and Hsiao K.-M. (2003) Autosomal dominant myotonia congenita in a Taiwanese family and beneficial response to mexiletine. J Acta Neurol. Taiwanica 12(3): 130-135.

12. H siao K.-M.*, Chen S.-S., Li S.-Y., Lin H.-M.,. Chiang S.-Y., Pan H., Huang C.-C., Kuo H.-C., Jou S.-B., Su C.-C., Ro L.-S., Liu C.-S., Lo M.-C., Chen C.-M., and Lin C.-C. (2003) Epidemiological and genetic studies of myotonic dystrophy type 1 in Taiwan. Neuroepidemiology 22(5):283-289. (SCI)

13. Pan H.*, Dung H.-N., Hsu H.-M., Hsiao K.-M., and Chen L.-Y. (2003) Cloning and developmental expression of p73 cDNA in zebrafish. Biochem Biophys Res Commun. 307(2):395-400. (SCI)

14. Pan H.*, Liao S.-J., Lai W.-Y., Lu H.-C., and Hsiao K.-M. (2002) Overexpression but lack of mutation and methylation of p73 in hepatocellular carcinoma. Acta Oncol. 41: 550-555. (SCI)

15. K uo H.-C., Huang C.-C.*, Chu C.-C., Wai Y.-Y., Chiang S.-Y., and Hsiao K.-M. (2002) Brain magnetic resonance images and molecular genetic analysis in myotonic dystrophy. J Acta Neurol. Taiwanica 11(4): 187-193.

16. H siao K.-M.* (2002) Reported relationship between increased CTG repeat lengths in myotonic dystrophy and azoospermia. Hum Reprod. 17(11):3004. (SCI)

17. H siao M.-C., Kuo H.-C., Huang C.-C.*, Chiang S.-Y., and Hsiao K.-M. (2002) A posterior fossa cystic lesion in myotonic dystrophy: report of a case. J Acta Neurol. Taiwanica 11(3): 144-148. (SCI)

18. Pan H., Li Y.-Y., Li T.-C., Tsai W.-T., Li S.-Y., and Hsiao K.-M.* (2002) Increased (CTG/CAG)n lengths in the myotonic dystrophy type 1 and Machado-Joseph disease genes in idiopathic azoospermia patients. Hum. Reprod. 17: 1578-1583. (SCI)

19. Pan H., Lin H.-M., Ku W.-Y., Li T.-C., Li S.-Y., Li C.-C., and Hsiao K.-M.* (2001). Haplotype analysis of the myotonic dystrophy type 1 (DM1) locus in Taiwan: implications for low prevalence and founder mutations of Taiwanese myotonic dystrophy type 1. Eu. J. Hum. Genet. 9: 638-641. (SCI)

20. P Jou S.-B., Lin H.-M., Pan H., Chiu Y.-L., Li S.-Y., and Hsiao K.-M.* (2001). Delineation of CTG repeats and clinical features in Taiwanese Myotonic Dystrophy family. Proc. Natl. Sci. Council, ROC. 25: 40-44.

 

B. 研討會論文

1.  Wang L.-C. and Hsiao K.-M. (2007) Reversibility of toxic effect mediated by expanded CUG and CAG repeat RNA in Caenorhabditis elegans. Fifteenth Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) p72 (P-08).

2.  Pan H., Hsu R.-J., Li C.-Y., and Hsiao K.-M. (2005) Long tract of untranslated CAG repeat is pathogenic in transgenic mice. The American Society of Human Genetics, 55th Annual Meeting (Salt lake City, USA). p405 (poster #2234).

3.  Hsiao K.-M., Chen K.-Y., Pan H., and Wang L.-C. (2005) Large untranslatable CAG repeats are pathogenic in vivo: using Caenorhabditis elegans as a model system. The American Society of Human Genetics, 55th Annual Meeting (Salt lake City, USA). p405 (poster #2233).

4.  2 Pan H., Hsu R.-J., Li C.-Y., and Hsiao K.-M. (2005) Long tract of untranslated CAG repeat is pathogenic in transgenic mice. The American Society of Human Genetics, 55th Annual Meeting (Salt lake City, USA). p405 (poster #2234).

5.  Chen K.-Y., Chiang S.-Y., Chen S.-D., and Hsiao K.-M. (2004) Differential muscular defects in transgenic Caenorhabditis elegans expressing distinct untranslatable trinucleotide repeats. Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) p61 (P-07).

6.  Chen K.-Y., Chiang S.-Y., Lin M.-J., Wu Y.-C., and Hsiao K.-M. (2003) Developmentally regulated effects of expanded CTG repeats on gene expression and neuromuscular function in Caenorhabditis elegans. Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) p116 (P-106).

7.  Chiang S.-Y., Li Y.-Y., Lin M.-J., Wu Y.-C., Pan H., and Hsiao K.-M. (2002)   Pathogenic effects of expanded CUG repeat in transgenic C. elegans. Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) p43 (A10).

8.  Chang L.-I., Jou S.-B., Huang C.-C., Kuo H.-C., Liao C.-H., and Hsiao K.-M. (2002) Identification of five novel mutations and one new polymorphism in the muscle chloride channel gene (CLCN1) in Taiwanese mytonia patients. Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) p63 (A44).

9.  Li Y.-Y., Tsai W.-T., Hsiao K.-M., and Pan H. (2001) A significant higher number of CAG repeats in the Machado-Joseph disease locus of myotonic dystrophy genome. Joint Annual Conference of Biomedical Sciences (Taiwan) 16:415.

10. Chiang S.-Y., Ku W.-Y., Pan H., and Hsiao K.-M. (2001) Myotonic dystrophy in Taiwan. Joint Annual Conference of Biomedical Sciences (Taiwan) 16:412.

11. Hsiao K.-M. (2001) Genetic analysis of myotonic dystrophy in Taiwan. 2nd Conference on biotechnology and molecular diagnosis (p13-17, invited speaker).

12. Tsai W.-T., Li Y.-Y., Hsiao K.-M., and Pan H. (2001) Comparison of (CAG/CTG)n frequency distribution at four disease loci in normal and azoospermia populations in Taiwan. Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) 9:52.

13. Ku W.-Y., Lin H.-M., Li T.-C., Li S.-Y., Pan H., and Hsiao K.-M. (2001) CTG repeat distribution and founder effect of the myotonic dystrophy mutation in Taiwan. Symposium on Recent Advances in Cellular and Molecular Biology (Taiwan) 9:52.

C. 專書

1. Hsiao K.-M. (2003) 分子檢驗專書第二部第十三章強直型肌肉萎縮症部分

2. Hsiao K.-M. (1995) Ph.D. thesis: Growth-regulated transcription from the mouse E2F1 promoter.

3. Hsiao K.-M. (1987) M.S. thesis: Production and characterization of N-acyl-D-amino acid amidohydrolase.