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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
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dc.contributor.author | Sheau-Leei Jin | en |
dc.contributor.author | 金曉蕾 | zh_TW |
dc.date.accessioned | 2021-07-01T08:15:19Z | - |
dc.date.available | 2021-07-01T08:15:19Z | - |
dc.date.issued | 1990 | |
dc.identifier.citation | Albert, D. D. M. (1987). Historic review of retinoblastoma. 94, 654-662. Angel, Deter (1988). The Jun proto-oncogene is positively autoregulated by its product, Jun/Ap-1. Cell, 55, 875-885. Beveren, C. V. et al. (1983). Analysis of FBJ-MuSV provirus and c-fos (Mouse) gene reveals that viral and cellular fos gene products different carboxy termini. Cell, 32, 1241-1255. Buchkovich, Karen et al. (1989). The retinoblastoma protein is prosphorylated during spceific phases of the cell cycle. Cell, 58, 1097-1105. Cooper, Jonathan A. and Peter Whyte (1989). RB and the cell cycle: eutrance or exit Cell, 58, 1009-1011. Cross, et al. (1989). Annu. Rev. Cell Blol. 5, 341-395. Decaprio, James A. et al. (1989). The product of the Retinoblastoma susceptibility gene has properties of a cell cycle regulatory element. Cell, 58, 1085-1095. Downward, Julian et al. (1988). P21ras-induced responsiveness of phosphatidylinositol turnover to bra dykinin is a receptor number effect. Biochemistry, 85, 5774-5778. Hansen, Marc F. (1988). Tumor suppressors: recrssive mutations that lead to cancer. Cell, 53, 172-173. Lamph, William W. et al. (1988). Induction of proto-oncogene Jun/Ap-1 by serum and TPA. Nature, 334. Ledwith, B. J. et al. (1990). Antisense-fos RNA causes partial reversion of the transformed phenotypes induced by the c-Ha-ras oncogene. Molecular and Cellular Biology, 10(4), 1545-1555. Lee, Wen-Hwa et al. (1987). Human retinoblastoma susceptibility gene: cloning identification and sequence. Science, 235, 1394-1399. Lee, Wen-Hwa et al. (1987). The retinoblastoma susceptibility gene encodes a nuclear phosphoprotein associated with PNA binding activity. Nature, 329, 642-645. Mulacahy, L. S., et al. (1985). Nature, 313, 241-243. Murphree, A. L., and Benedict W. F. (1984). Science, 223, 1028-1033. Naka beppu, Yusakn et al. (1988). DNA binding activities of three musine jan proteins: stimulation by Fos. Cell, 55, 907-915. Rauscher, Frank J. et al. (1988). Fos-associated protein P39 is the product of the jan proto-oncogene. Science, 240, 1010-1016. Strunl Kevin (1988). The Jun oncoprotein, a vertebrate transcription factor, activates transcription in yeast. Nature, 332, 649-650. Trimble, W. S. et al. (1986). Inducible cellular transformation by a metallothioneinras hybrid oncogene leads to nature killer cell susceptibility. Nature, 321, 782-784. Wilson, Tim and Richard Treisman (1988). Fos C-terminal mutations block down-regulation of C-fos transcription following serum stimulation. EMBO, 7, 4193-4202. Voge, Peter K. and Timothy J. Bos (1989). The oncogene jun and nuclear signalling. TIBS, 14, 172-175. Yamada, H. et al. (1990). Isolation of recessive (meditor) revertant from NIH 3T3 cells transformed with a c-H-ras oncogene. Molecular and Cellular Biology, 10(4), 1822-1827. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/75778 | - |
dc.description.abstract | 細胞生長所受精確控制的複雜性是目前許多生化學家所急欲探討的問題,雖然綜合目前研究所知,對細胞生長調控的大概圖繪略知一二,但仍無法完全速結所有線索與問題來窺探全貌。 目前發現一些proto-oncogene和anti-oncogene本身基因產物就具有生長素(growth factor)或一些生長素的變質接受器(receptor)或訊息傳遞的仲價者(mediator)等等功能,直接參與調控細胞生長機制。而且也發現當這些基因的產物發生突變(mutaion)或截短(deletion)而失去功能時,會使得細胞生長失控,甚至轉化為癌化細胞。所以用這些基因來當作研究細胞生長控制機制的探針是很好的研究方向。 本實驗在賴老師指導和素材的提供下,設計了一些以proto-oncogene(fos, jun, vas)和anti-oncogene (Rb)做為探針,來探討正常老鼠纖維細胞(NIH 3T3)和癌化老鼠細胞(B104-l)在這些重要基因產物供應失調下,有何不同的結果,而可以得到那些重要消息。所以本實驗第一步驟即將NIH 3T3和B104-1細胞分別做serum starvation 48小時,再將細胞的培養基換成含有20%FCS的培養基做serum stimulation 0.5;1;2;6小時後,再用GTC方法抽取實驗組細胞的RNA跑formaldehyde gel,然後分別以具有放射性的fos, jun, ras, Rb的DNA片段做探針,來分析NIH 3T3和B 104-1在dos, jun, ras, Rb的基因上表現有何不同。結果NIH 3T3的fos和jun在serum stimulation 0.5?1hr.之後基因有明顯大量表現;但在B104-1則可以看到fos,jun的基因表現量不受serum stimulation影響,而一直維持在一定量上。可是,即使在B104-1的control組(沒進行血清starvation)發現B104-1的jun表現比NIH 3T3的多5?6倍,是否暗示在neu transform過後歿B104-1會影響到jun的表現量?或表示neu和jun之間有什麼相互關係?則有待進一步的研究。另外,ras和Rb不論是在NIH 3T3或B 104-1中,其基因表現量皆不受血清的刺激而有所改變。 至於實驗第二部份,基本上是設計反順序Rb,使其能正常的在NIH 3T3和B104-1細胞中表現大量的反順序Rb,而有效的抑制NIH 3T3和B104-l細胞內RB產物的表現量。看看對細胞生長循環調控扮演重要角色的RB,在低量或缺乏的狀況下,正常細胞NIH 3T3的生長調控是否會脫離正常路途?結果在細胞生長線(Cell groth curve)上有反順序Rb(anti-Rb)成功表現的細胞,不論是在NIH 3T3或B104-1都比正常細胞來得快。但在soft agar實驗分析上,有表現反順序Rb的細胞,其癌化能力在NIH 3T3和B 104-1並沒有明顯增加的現象。 | zh_TW |
dc.description.provenance | Made available in DSpace on 2021-07-01T08:15:19Z (GMT). No. of bitstreams: 0 Previous issue date: 1990 | en |
dc.description.tableofcontents | 摘要. . . . . . . . . . . . 1 簡介. . . . . . . . . . . . 3 實驗步驟. . . . . . . . . . . . 8 結果. . . . . . . . . . . .13 討論. . . . . . . . . . . . 16 表. . . . . . . . . . . . 20 圖. . . . . . . . . . . . 22 引用文獻. . . . . . . . . . . . 35 | |
dc.language.iso | zh-TW | |
dc.title | Anti-sence RB 對細胞生長之研究 | zh_TW |
dc.title | The Effect of Anti-sence RB to Cell Growth | en |
dc.date.schoolyear | 78-2 | |
dc.description.degree | 碩士 | |
dc.relation.page | 40 | |
dc.rights.note | 未授權 | |
dc.contributor.author-dept | 生命科學院 | zh_TW |
dc.contributor.author-dept | 生化科學研究所 | zh_TW |
顯示於系所單位: | 生化科學研究所 |
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