請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/26493完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 蔡錦華(Ching-Hwa Tsai) | |
| dc.contributor.author | Pei-Lun Weng | en |
| dc.contributor.author | 翁培倫 | zh_TW |
| dc.date.accessioned | 2021-06-08T07:12:24Z | - |
| dc.date.copyright | 2008-09-11 | |
| dc.date.issued | 2008 | |
| dc.date.submitted | 2008-07-31 | |
| dc.identifier.citation | 1. Amit, I., L. Yakir, M. Katz, Y. Zwang, M. D. Marmor, A. Citri, K. Shtiegman, I. Alroy, S. Tuvia, Y. Reiss, E. Roubini, M. Cohen, R. Wides, E. Bacharach, U. Schubert, and Y. Yarden. 2004. Tal, a Tsg101-specific E3 ubiquitin ligase, regulates receptor endocytosis and retrovirus budding. Genes Dev 18:1737-52.
2. Bentley, D. L. 2005. Rules of engagement: co-transcriptional recruitment of pre-mRNA processing factors. Curr Opin Cell Biol 17:251-6. 3. Bishop, N., and P. Woodman. 2001. TSG101/mammalian VPS23 and mammalian VPS28 interact directly and are recruited to VPS4-induced endosomes. J Biol Chem 276:11735-42. 4. Bouamr, F., J. A. Melillo, M. Q. Wang, K. Nagashima, M. de Los Santos, A. Rein, and S. P. Goff. 2003. PPPYVEPTAP motif is the late domain of human T-cell leukemia virus type 1 Gag and mediates its functional interaction with cellular proteins Nedd4 and Tsg101 [corrected]. J Virol 77:11882-95. 5. Brinkman, B. M. 2004. Splice variants as cancer biomarkers. Clin Biochem 37:584-94. 6. Burgdorf, S., P. Leister, and K. H. Scheidtmann. 2004. TSG101 interacts with apoptosis-antagonizing transcription factor and enhances androgen receptor-mediated transcription by promoting its monoubiquitination. J Biol Chem 279:17524-34. 7. Caceres, J. F., and A. R. Kornblihtt. 2002. Alternative splicing: multiple control mechanisms and involvement in human disease. Trends Genet 18:186-93. 8. Carlton, J. G., and J. Martin-Serrano. 2007. Parallels between cytokinesis and retroviral budding: a role for the ESCRT machinery. Science 316:1908-12. 9. Chalfant, C. E., K. Rathman, R. L. Pinkerman, R. E. Wood, L. M. Obeid, B. Ogretmen, and Y. A. Hannun. 2002. De novo ceramide regulates the alternative splicing of caspase 9 and Bcl-x in A549 lung adenocarcinoma cells. Dependence on protein phosphatase-1. J Biol Chem 277:12587-95. 10. Chen, Y. J., P. H. Chen, S. Y. Lin, and J. G. Chang. 1999. Analysis of aberrant transcription of TSG101 in hepatocellular carcinomas. Eur J Cancer 35:302-8. 11. Chua, H. H., H. H. Lee, S. S. Chang, C. C. Lu, T. H. Yeh, T. Y. Hsu, T. H. Cheng, J. T. Cheng, M. R. Chen, and C. H. Tsai. 2007. Role of the TSG101 gene in Epstein-Barr virus late gene transcription. J Virol 81:2459-71. 12. Deng, Y. F., F. Tian, Y. D. Lu, Z. C. Chen, D. H. Xie, X. M. Yang, and X. Y. Shao. 2001. Mutation and abnormal expression of the fragile histidine triad gene in nasopharyngeal carcinoma. Laryngoscope 111:1589-92. 13. Di Fiore, P. P., S. Polo, and K. Hofmann. 2003. When ubiquitin meets ubiquitin receptors: a signalling connection. Nat Rev Mol Cell Biol 4:491-7. 14. Fang, S., and A. M. Weissman. 2004. A field guide to ubiquitylation. Cell Mol Life Sci 61:1546-61. 15. Faustino, N. A., and T. A. Cooper. 2003. Pre-mRNA splicing and human disease. Genes Dev 17:419-37. 16. Freemont, P. S. 2000. RING for destruction? Curr Biol 10:R84-7. 17. Garcia-Blanco, M. A., A. P. Baraniak, and E. L. Lasda. 2004. Alternative splicing in disease and therapy. Nat Biotechnol 22:535-46. 18. Garrus, J. E., U. K. von Schwedler, O. W. Pornillos, S. G. Morham, K. H. Zavitz, H. E. Wang, D. A. Wettstein, K. M. Stray, M. Cote, R. L. Rich, D. G. Myszka, and W. I. Sundquist. 2001. Tsg101 and the vacuolar protein sorting pathway are essential for HIV-1 budding. Cell 107:55-65. 19. Ghigna, C., M. Moroni, C. Porta, S. Riva, and G. Biamonti. 1998. Altered expression of heterogenous nuclear ribonucleoproteins and SR factors in human colon adenocarcinomas. Cancer Res 58:5818-24. 20. Ghosh, A., D. Stewart, and G. Matlashewski. 2004. Regulation of human p53 activity and cell localization by alternative splicing. Mol Cell Biol 24:7987-97. 21. Giglio, S., F. Mancini, F. Gentiletti, G. Sparaco, L. Felicioni, F. Barassi, C. Martella, A. Prodosmo, S. Iacovelli, F. Buttitta, A. Farsetti, S. Soddu, A. Marchetti, A. Sacchi, A. Pontecorvi, and F. Moretti. 2005. Identification of an aberrantly spliced form of HDMX in human tumors: a new mechanism for HDM2 stabilization. Cancer Res 65:9687-94. 22. Haglund, K., and I. Dikic. 2005. Ubiquitylation and cell signaling. EMBO J 24:3353-9. 23. Haglund, K., S. Sigismund, S. Polo, I. Szymkiewicz, P. P. Di Fiore, and I. Dikic. 2003. Multiple monoubiquitination of RTKs is sufficient for their endocytosis and degradation. Nat Cell Biol 5:461-6. 24. Hershko, A., and A. Ciechanover. 1998. The ubiquitin system. Annu Rev Biochem 67:425-79. 25. Hicke, L. 2001. Protein regulation by monoubiquitin. Nat Rev Mol Cell Biol 2:195-201. 26. Hochstrasser, M. 1995. Ubiquitin, proteasomes, and the regulation of intracellular protein degradation. Curr Opin Cell Biol 7:215-23. 27. Huibregtse, J. M., M. Scheffner, S. Beaudenon, and P. M. Howley. 1995. A family of proteins structurally and functionally related to the E6-AP ubiquitin-protein ligase. Proc Natl Acad Sci U S A 92:2563-7. 28. Joazeiro, C. A., and A. M. Weissman. 2000. RING finger proteins: mediators of ubiquitin ligase activity. Cell 102:549-52. 29. Johnson, E. S., P. C. Ma, I. M. Ota, and A. Varshavsky. 1995. A proteolytic pathway that recognizes ubiquitin as a degradation signal. J Biol Chem 270:17442-56. 30. Johnson, J. M., J. Castle, P. Garrett-Engele, Z. Kan, P. M. Loerch, C. D. Armour, R. Santos, E. E. Schadt, R. Stoughton, and D. D. Shoemaker. 2003. Genome-wide survey of human alternative pre-mRNA splicing with exon junction microarrays. Science 302:2141-4. 31. Kim, B. Y., J. A. Olzmann, G. S. Barsh, L. S. Chin, and L. Li. 2007. Spongiform neurodegeneration-associated E3 ligase Mahogunin ubiquitylates TSG101 and regulates endosomal trafficking. Mol Biol Cell 18:1129-42. 32. Kim, H. T., K. P. Kim, F. Lledias, A. F. Kisselev, K. M. Scaglione, D. Skowyra, S. P. Gygi, and A. L. Goldberg. 2007. Certain pairs of ubiquitin-conjugating enzymes (E2s) and ubiquitin-protein ligases (E3s) synthesize nondegradable forked ubiquitin chains containing all possible isopeptide linkages. J Biol Chem 282:17375-86. 33. Klaes, R., M. Kloor, F. Willeke, P. Melsheimer, M. von Knebel Doeberitz, and R. Ridder. 1999. Significant increase of a specific variant TSG101 transcript during the progression of cervical neoplasia. Eur J Cancer 35:733-7. 34. Koon, N., R. Schneider-Stock, M. Sarlomo-Rikala, J. Lasota, M. Smolkin, G. Petroni, A. Zaika, C. Boltze, F. Meyer, L. Andersson, S. Knuutila, M. Miettinen, and W. El-Rifai. 2004. Molecular targets for tumour progression in gastrointestinal stromal tumours. Gut 53:235-40. 35. Koonin, E. V., and R. A. Abagyan. 1997. TSG101 may be the prototype of a class of dominant negative ubiquitin regulators. Nat Genet 16:330-1. 36. Kornblihtt, A. R. 2005. Promoter usage and alternative splicing. Curr Opin Cell Biol 17:262-8. 37. Kornblihtt, A. R., M. de la Mata, J. P. Fededa, M. J. Munoz, and G. Nogues. 2004. Multiple links between transcription and splicing. RNA 10:1489-98. 38. Krempler, A., M. D. Henry, A. A. Triplett, and K. U. Wagner. 2002. Targeted deletion of the Tsg101 gene results in cell cycle arrest at G1/S and p53-independent cell death. J Biol Chem 277:43216-23. 39. Lee, M. P., and A. P. Feinberg. 1997. Aberrant splicing but not mutations of TSG101 in human breast cancer. Cancer Res 57:3131-4. 40. Li, L., and S. N. Cohen. 1996. Tsg101: a novel tumor susceptibility gene isolated by controlled homozygous functional knockout of allelic loci in mammalian cells. Cell 85:319-29. 41. Li, L., X. Li, U. Francke, and S. N. Cohen. 1997. The TSG101 tumor susceptibility gene is located in chromosome 11 band p15 and is mutated in human breast cancer. Cell 88:143-54. 42. Lin, C. T., W. Y. Chan, W. Chen, H. M. Huang, H. C. Wu, M. M. Hsu, S. M. Chuang, and C. C. Wang. 1993. Characterization of seven newly established nasopharyngeal carcinoma cell lines. Lab Invest 68:716-27. 43. Liu, H. X., L. Cartegni, M. Q. Zhang, and A. R. Krainer. 2001. A mechanism for exon skipping caused by nonsense or missense mutations in BRCA1 and other genes. Nat Genet 27:55-8. 44. Liu, R. T., C. C. Huang, H. L. You, F. F. Chou, C. C. Hu, F. P. Chao, C. M. Chen, and J. T. Cheng. 2002. Overexpression of tumor susceptibility gene TSG101 in human papillary thyroid carcinomas. Oncogene 21:4830-7. 45. Lo, Y. F., T. C. Chen, S. C. Chen, and C. C. Chao. 2000. Aberrant expression of TSG101 in Taiwan Chinese breast cancer. Breast Cancer Res Treat 60:259-66. 46. Lu, Q., L. W. Hope, M. Brasch, C. Reinhard, and S. N. Cohen. 2003. TSG101 interaction with HRS mediates endosomal trafficking and receptor down-regulation. Proc Natl Acad Sci U S A 100:7626-31. 47. Lukas, J., D. Q. Gao, M. Keshmeshian, W. H. Wen, D. Tsao-Wei, S. Rosenberg, and M. F. Press. 2001. Alternative and aberrant messenger RNA splicing of the mdm2 oncogene in invasive breast cancer. Cancer Res 61:3212-9. 48. Ma, X. R., U. H. Edmund Sim, B. Pauline, L. Patricia, and J. Rahman. 2008. Overexpression of WNT2 and TSG101 genes in colorectal carcinoma. Trop Biomed 25:46-57. 49. Maniatis, T., and R. Reed. 2002. An extensive network of coupling among gene expression machines. Nature 416:499-506. 50. Martin-Serrano, J., A. Yarovoy, D. Perez-Caballero, and P. D. Bieniasz. 2003. Divergent retroviral late-budding domains recruit vacuolar protein sorting factors by using alternative adaptor proteins. Proc Natl Acad Sci U S A 100:12414-9. 51. Martin-Serrano, J., T. Zang, and P. D. Bieniasz. 2001. HIV-1 and Ebola virus encode small peptide motifs that recruit Tsg101 to sites of particle assembly to facilitate egress. Nat Med 7:1313-9. 52. Mazoyer, S., N. Puget, L. Perrin-Vidoz, H. T. Lynch, O. M. Serova-Sinilnikova, and G. M. Lenoir. 1998. A BRCA1 nonsense mutation causes exon skipping. Am J Hum Genet 62:713-5. 53. McDonald, B., and J. Martin-Serrano. 2008. Regulation of Tsg101 Expression by the Steadiness Box: A Role of Tsg101-associated Ligase. Mol Biol Cell 19:754-63. 54. Modrek, B., and C. Lee. 2002. A genomic view of alternative splicing. Nat Genet 30:13-9. 55. Moyret-Lalle, C., C. Duriez, J. Van Kerckhove, C. Gilbert, Q. Wang, and A. Puisieux. 2001. p53 induction prevents accumulation of aberrant transcripts in cancer cells. Cancer Res 61:486-8. 56. Mukhopadhyay, D., and H. Riezman. 2007. Proteasome-independent functions of ubiquitin in endocytosis and signaling. Science 315:201-5. 57. Muromoto, R., K. Sugiyama, T. Yamamoto, K. Oritani, K. Shimoda, and T. Matsuda. 2004. Physical and functional interactions between Daxx and TSG101. Biochem Biophys Res Commun 316:827-33. 58. Oh, Y., M. L. Proctor, Y. H. Fan, L. K. Su, W. K. Hong, K. M. Fong, Y. S. Sekido, A. F. Gazdar, J. D. Minna, and L. Mao. 1998. TSG101 is not mutated in lung cancer but a shortened transcript is frequently expressed in small cell lung cancer. Oncogene 17:1141-8. 59. Peng, J., D. Schwartz, J. E. Elias, C. C. Thoreen, D. Cheng, G. Marsischky, J. Roelofs, D. Finley, and S. P. Gygi. 2003. A proteomics approach to understanding protein ubiquitination. Nat Biotechnol 21:921-6. 60. Proudfoot, N. J., A. Furger, and M. J. Dye. 2002. Integrating mRNA processing with transcription. Cell 108:501-12. 61. Sharp, P. A. 1994. Split genes and RNA splicing. Cell 77:805-15. 62. Shen, H., Y. Pan, Z. Han, L. Hong, N. Liu, S. Han, L. Yao, H. Xie, C. Zhaxi, Y. Shi, and D. Fan. 2004. Reversal of multidrug resistance of gastric cancer cells by downregulation of TSG101 with TSG101siRNA. Cancer Biol Ther 3:561-5. 63. Steinman, H. A., E. Burstein, C. Lengner, J. Gosselin, G. Pihan, C. S. Duckett, and S. N. Jones. 2004. An alternative splice form of Mdm2 induces p53-independent cell growth and tumorigenesis. J Biol Chem 279:4877-86. 64. Stickeler, E., F. Kittrell, D. Medina, and S. M. Berget. 1999. Stage-specific changes in SR splicing factors and alternative splicing in mammary tumorigenesis. Oncogene 18:3574-82. 65. Stuchell, M. D., J. E. Garrus, B. Muller, K. M. Stray, S. Ghaffarian, R. McKinnon, H. G. Krausslich, S. G. Morham, and W. I. Sundquist. 2004. The human endosomal sorting complex required for transport (ESCRT-I) and its role in HIV-1 budding. J Biol Chem 279:36059-71. 66. Sun, Z., J. Pan, W. X. Hope, S. N. Cohen, and S. P. Balk. 1999. Tumor susceptibility gene 101 protein represses androgen receptor transactivation and interacts with p300. Cancer 86:689-96. 67. Tamborini, E., G. Della Torre, C. Lavarino, A. Azzarelli, P. Carpinelli, M. A. Pierotti, and S. Pilotti. 2001. Analysis of the molecular species generated by MDM2 gene amplification in liposarcomas. Int J Cancer 92:790-6. 68. Tarn, W. Y., and J. A. Steitz. 1996. A novel spliceosome containing U11, U12, and U5 snRNPs excises a minor class (AT-AC) intron in vitro. Cell 84:801-11. 69. Tennyson, C. N., H. J. Klamut, and R. G. Worton. 1995. The human dystrophin gene requires 16 hours to be transcribed and is cotranscriptionally spliced. Nat Genet 9:184-90. 70. Venables, J. P. 2004. Aberrant and alternative splicing in cancer. Cancer Res 64:7647-54. 71. Venables, J. P. 2006. Unbalanced alternative splicing and its significance in cancer. Bioessays 28:378-86. 72. VerPlank, L., F. Bouamr, T. J. LaGrassa, B. Agresta, A. Kikonyogo, J. Leis, and C. A. Carter. 2001. Tsg101, a homologue of ubiquitin-conjugating (E2) enzymes, binds the L domain in HIV type 1 Pr55(Gag). Proc Natl Acad Sci U S A 98:7724-9. 73. Wagner, K. U., P. Dierisseau, E. B. Rucker, 3rd, G. W. Robinson, and L. Hennighausen. 1998. Genomic architecture and transcriptional activation of the mouse and human tumor susceptibility gene TSG101: common types of shorter transcripts are true alternative splice variants. Oncogene 17:2761-70. 74. Wagner, K. U., A. Krempler, Y. Qi, K. Park, M. D. Henry, A. A. Triplett, G. Riedlinger, I. E. Rucker, and L. Hennighausen. 2003. Tsg101 is essential for cell growth, proliferation, and cell survival of embryonic and adult tissues. Mol Cell Biol 23:150-62. 75. Watanabe, M., Y. Yanagi, Y. Masuhiro, T. Yano, H. Yoshikawa, J. Yanagisawa, and S. Kato. 1998. A putative tumor suppressor, TSG101, acts as a transcriptional suppressor through its coiled-coil domain. Biochem Biophys Res Commun 245:900-5. 76. Wollerton, M. C., C. Gooding, E. J. Wagner, M. A. Garcia-Blanco, and C. W. Smith. 2004. Autoregulation of polypyrimidine tract binding protein by alternative splicing leading to nonsense-mediated decay. Mol Cell 13:91-100. 77. Yanagida-Ishizaki, Y., T. Takei, R. Ishizaki, H. Imakagura, S. Takahashi, H. W. Shin, Y. Katoh, and K. Nakayama. 2008. Recruitment of Tom1L1/Srcasm to endosomes and the midbody by Tsg101. Cell Struct Funct 33:91-100. 78. Yin, Y., C. W. Stephen, M. G. Luciani, and R. Fahraeus. 2002. p53 Stability and activity is regulated by Mdm2-mediated induction of alternative p53 translation products. Nat Cell Biol 4:462-7. 79. You, H. L., H. L. Eng, S. F. Hsu, C. M. Chen, T. C. Ye, W. T. Liao, M. Y. Huang, R. Baer, and J. T. Cheng. 2007. A PKC-Sp1 signaling pathway induces early differentiation of human keratinocytes through upregulation of TSG101. Cell Signal 19:1201-11. 80. Young, T. W., F. C. Mei, D. G. Rosen, G. Yang, N. Li, J. Liu, and X. Cheng. 2007. Up-regulation of tumor susceptibility gene 101 protein in ovarian carcinomas revealed by proteomics analyses. Mol Cell Proteomics 6:294-304. 81. Zerbe, L. K., I. Pino, R. Pio, P. F. Cosper, L. D. Dwyer-Nield, A. M. Meyer, J. D. Port, L. M. Montuenga, and A. M. Malkinson. 2004. Relative amounts of antagonistic splicing factors, hnRNP A1 and ASF/SF2, change during neoplastic lung growth: implications for pre-mRNA processing. Mol Carcinog 41:187-96. 82. Zhong, Q., Y. Chen, D. Jones, and W. H. Lee. 1998. Perturbation of TSG101 protein affects cell cycle progression. Cancer Res 58:2699-702. 83. Zhu, G., R. Gilchrist, N. Borley, H. W. Chng, M. Morgan, J. F. Marshall, R. S. Camplejohn, G. H. Muir, and I. R. Hart. 2004. Reduction of TSG101 protein has a negative impact on tumor cell growth. Int J Cancer 109:541-7. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/26493 | - |
| dc.description.abstract | 腫瘤易感基因101 (Tumor susceptibility gene 101，TSG101)，首先利用老鼠纖維母細胞 (fibroblast) 進行heterozygous knockout strategy中所篩選出來，如今被認為反而與細胞癌化有著顯著的關連性。先前研究發現TSG101為細胞生長所必需，並且也在某些惡性腫瘤細胞當中可見到TSG101表現量有上升之情況。除此之外，TSG101在內體運輸、細胞質分裂、調控細胞內基因表現和病毒出芽均扮演重要的角色。在惡性腫瘤細胞當中可發現tsg101基因並不會發生基因序列上之突變，但卻會因為選擇性剪接產生不同之mRNA isoform並且更進一步也証實某些特定的isoform與腫瘤的發展有著極重要的關連性。根據本實驗室先前的研究發現，在鼻咽癌組織中可偵測到一特定選擇性剪接之產物TSGΔ154-1054，但在非惡性細胞之淋巴增生組織則不會偵測到，另外也發現在表現TSGΔ154-1054之鼻咽癌組織當中TSG101表現量也有上升的情形，因此本篇研究主要著重於TSGΔ154-1054之表現與TSG101表現之關係。利用短期轉染實驗，可見TSGΔ154-1054影響TSG101表現是透過轉譯層次而非轉錄層次。在pulse-chase和cycloheximide-chase實驗中證實TSG101表現量上升並非增加TSG101之新生合成而是延長其半衰期，除此之外，將TSGΔ154-1054之起始密碼ATG置換成AAA後，TSGΔ154-1054無法轉譯成蛋白質其延長TSG101半衰期之能力也隨之失去，証實了TSGΔ154-1054影響了TSG101表現是透過其蛋白質產物。進一步分析，TSGΔ154-1054可藉由與TSG101競爭和Tal之結合，進而防止了TSG101降解，而延長了TSG101之半衰期。最後亦證實了TSGΔ154-1054可以藉由增加TSG101的表現量促進細胞的增生和腫瘤的生成。 | zh_TW |
| dc.description.abstract | Tumor susceptibility gene 101 (TSG101) was originally discovered in screening potent tumor suppressor gene using heterozygous knockout strategy in mouse fibroblasts models. Rather, this gene is now being regarded with oncogenic potency. Previous studies have suggested that TSG101 is required for cell growth and proliferation, and is over-expressed in some human cancer cells. In addition, TSG101 also plays a crucial role in endosomal trafficking, cytokinesis, transcriptional regulation of cellular genes and virion budding. Although the genomic mutation of TSG101 is not founded in cancerous tissues, the alternative splicing patterns of TSG101 pre-mRNA has been identified in various human cancers. Of note, the alternative splicing isoform TSGΔ154-1054 (a deleted fragment in TSG101 nucleotides 154-1054) strongly correlated with tumor progression and advanced tumor stages. In our previous studies, the over-expression of TSGΔ154-1054 was found in nasopharyngeal carcinomas (NPC) biopsies but not in lymphoid hyperplasia (LH) control tissues. In addition, the strong correlation of over-expression of TSGΔ154-1054 and up-regulation of TSG101 protein was found in NPC biopsies. So, the relationship between over-expression of TSGΔ154-1054 and TSG101 protein expression level is the target issue in this study.
In transfection assay, we found that expression of TSGΔ154-1054 enhances the expression of TSG101 at protein level but not transcrional level. In cycloheximide experiment, TSGΔ154-1054 prolongs TSG101 half-life. Data from TSGΔ154-1054 start codon mutant assay indicated that protein product of TSGΔ154-1054 is required for its ability of prolonging TSG101 half-life. Mechanistically, TSGΔ154-1054 competing with TSG101 from binding TSG101-specific E3 ubiquitin ligase (Tal) impairs the TSG101 proteasome degradation and thus prolonging TSG101 protein half-life. Of note, the biological consequences of expression of TSGΔ154-1054 are promoting cell proliferation and enhancing tumor oncogenecity. To our knowledge, this is the first study to reveal the relationship between TSG101 and its alternative splicing variant TSGΔ154-1054. Also, this is the first study to show the biological influence of alternative splicing variant TSGΔ154-1054 on cell proliferation and tumor formation via enhancement the stabilizing of its wild type TSG101 proetin. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-08T07:12:24Z (GMT). No. of bitstreams: 1 ntu-97-R95445111-1.pdf: 3159122 bytes, checksum: 833e0ae4c0271a478de14d0b0ebf201f (MD5) Previous issue date: 2008 | en |
| dc.description.tableofcontents | 中文摘要.................................................Ⅰ
英文摘要.................................................Ⅱ 序論......................................................1 實驗目的.................................................10 實驗材料與方法...........................................11 實驗結果.................................................28 討論.....................................................38 圖.......................................................42 附圖.....................................................70 附表.....................................................79 參考文獻................................................81 | |
| dc.language.iso | zh-TW | |
| dc.subject | 剪接變異體 | zh_TW |
| dc.subject | 腫瘤易感基因101 | zh_TW |
| dc.subject | aberrant splicing | en |
| dc.subject | TSG101 | en |
| dc.title | 剪接變異體產物TSGΔ154-1054對TSG101
蛋白質穩定性與生物功能之影響 | zh_TW |
| dc.title | Novel effect of aberrant splicing variant TSGΔ154-1054 on
TSG101 protein stability and biological activity | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 96-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 陳美如(Mei-Ru Chen),許金玉(Jin-Yuh Shew),呂仁(Jean Lu) | |
| dc.subject.keyword | 腫瘤易感基因101,剪接變異體, | zh_TW |
| dc.subject.keyword | TSG101,aberrant splicing, | en |
| dc.relation.page | 87 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2008-07-31 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| 顯示於系所單位： | 微生物學科所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-97-1.pdf 未授權公開取用 | 3.09 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。