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【reintroduction efforts】

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大家好,小豆豆來為大家解答以上的問題。reintroduction efforts這個很多人還不知道,現在讓我們一起來看看吧！
1、這是發表在Nature上的一篇文章《The common biology of cancer and ageing》中的話，原文是這樣的——“Most adult cells have limiting amounts of telomerase that are not sufficient to prevent telomere loss, resulting in the shortening of telomeres with age[53]. As telomeres are essential for chromosomal stability, this progressive telomere loss was proposed to be at the basis of cellular senescence and ageing in the ‘telomere hypothesis’[53]. Indeed, telomere length has been shown to predict the replicative capacity of human cells and the appearance of certain age-associated pathologies in humans[54,55]. The final demonstration that telomere shortening was one of the causes of cellular senescence came from the observation that re-introduction of the TERT telomerase gene was sufficient to bypass replicative senescence and to confer immortal growth on a number of human primary cell lines[56]. Furthermore, the generation and characterization of the telomerase knockout mouse model has been instrumental in demonstrating that short telomeres result in multiple organismal defects caused by defective tissue regeneration[57–59]. In particular, telomerase-deficient mice with short telomeres show reduced function of various stem cell compartments including those in the bone marrow and skin[58,60]. Interestingly, patients who have inherited or acquired genetic defects that limit telomere maintenance seem to be at substantially increased risk of a range of conditions including aplastic anaemia61, idiopathic pulmonary fibrosis[62,63] and the rarer dyskeratosis congenita syndrome[64]”.你所提供的語句在文中參考文獻是56，也就是1998年發表在Science上的一篇文章《Extension of Life-Span by Introduction of Telomerase into Normal Human Cells》，這里附上文章摘要：“Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced staining for -galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine”，從中我們可以看出作者研究的對象是不含端粒酶的兩個正常人細胞型，通過向這兩個細胞型引入含有端粒酶編碼基因的表達載體補足了端粒酶缺失導致的端粒縮短等現象也就說明了端粒酶的存在對于細胞的正常生長及傳代是必須的。
2、如果你需要相應參照文獻可以與jingboduan@聯系。
3、意思是將逆轉錄端粒酶基因轉入人的細胞（成纖維細胞、視網膜色素細胞等）,獲得永生的細胞系。
4、你問的問題是如何將該基因轉入人體細胞，應用逆轉錄病毒載體是最高效的方法。
本文到此分享完畢，希望對大家有所幫助。