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细胞衰老过程中的基因修饰。

Genetic modifications during cellular aging.

作者信息

Goldstein S, Shmookler Reis R J

出版信息

Mol Cell Biochem. 1984 Sep;64(1):15-30. doi: 10.1007/BF00420924.

DOI:10.1007/BF00420924
PMID:6387441
Abstract

We review evidence that biological aging is a genetic process related to development and cytodifferentiation and thus may involve alterations of DNA structure and gene expression. We conclude that although determined to a high degree aging also involves stochastic features which lead to progressive somatic cell diversification during the life span. These considerations may help to explain the unevenness of physiological decline and the clonal emergence of certain age-dependent diseases such as cancer.

摘要

我们回顾了相关证据,即生物衰老乃是一个与发育及细胞分化相关的遗传过程,因而可能涉及DNA结构和基因表达的改变。我们得出结论,尽管衰老在很大程度上由基因决定,但它也具有随机特征,这些特征会在生命周期中导致体细胞逐渐多样化。这些考量或许有助于解释生理衰退的不均衡性以及某些与年龄相关疾病(如癌症)的克隆性出现。

相似文献

1
Genetic modifications during cellular aging.细胞衰老过程中的基因修饰。
Mol Cell Biochem. 1984 Sep;64(1):15-30. doi: 10.1007/BF00420924.
2
Alterations in genome structure and expression in aging human fibroblasts.
Prog Clin Biol Res. 1985;195:1-14.
3
Transcription and replication of mitochondrial DNA.线粒体DNA的转录与复制。
Hum Reprod. 2000 Jul;15 Suppl 2:11-7. doi: 10.1093/humrep/15.suppl_2.11.
4
Mitochondrial DNA structure and function.线粒体DNA的结构与功能。
Int Rev Neurobiol. 2002;53:3-23. doi: 10.1016/s0074-7742(02)53002-6.
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Elements which stimulate gene amplification in mammalian cells: role of recombinogenic sequences/structures and transcriptional activation.刺激哺乳动物细胞基因扩增的元件:重组序列/结构和转录激活的作用。
Nucleic Acids Res. 1991 May 11;19(9):2477-84. doi: 10.1093/nar/19.9.2477.
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How Far Can Mitochondrial DNA Drive the Disease?线粒体 DNA 能在多大程度上引发疾病?
Adv Exp Med Biol. 2017;1038:1-8. doi: 10.1007/978-981-10-6674-0_1.
7
[Repeated DNA sequences as an engine of biological diversification].[重复DNA序列作为生物多样性的驱动力]
Mol Biol (Mosk). 2011 Sep-Oct;45(5):765-92.
8
[DNA structure and cell transformation].[DNA结构与细胞转化]
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A hypothesis on the action of chromosomal genes.
J Theor Biol. 1984 Jun 21;108(4):645-61.
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Frequency of replication/transcription errors in (A)/(T) runs of human genes.人类基因(A)/(T)序列中复制/转录错误的频率。
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引用本文的文献

1
Specific growth inhibitory sequences in genomic DNA from quiescent human embryo fibroblasts.来自静止期人类胚胎成纤维细胞基因组DNA中的特异性生长抑制序列。
Mol Cell Biol. 1987 May;7(5):1894-9. doi: 10.1128/mcb.7.5.1894-1899.1987.
2
Loss of expression of a differentiated function gene, steroid 17 alpha-hydroxylase, as adrenocortical cells senescence in culture.随着培养的肾上腺皮质细胞衰老,分化功能基因类固醇17α-羟化酶的表达丧失。
Proc Natl Acad Sci U S A. 1987 Mar;84(6):1580-4. doi: 10.1073/pnas.84.6.1580.
3
Frequency of 6-thioguanine-resistant T cells is inversely related to the declining T-cell activities in aging mice.

本文引用的文献

1
ON THE NATURE OF THE AGING PROCESS.论衰老过程的本质。
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AN ESTIMATE OF THE MUTATIONAL DAMAGE IN MAN FROM DATA ON CONSANGUINEOUS MARRIAGES.根据近亲婚姻数据对人类突变损伤的估计
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A STOCHASTIC MODEL OF STEM CELL PROLIFERATION, BASED ON THE GROWTH OF SPLEEN COLONY-FORMING CELLS.基于脾集落形成细胞生长的干细胞增殖随机模型
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Regulation of mRNA polyadenylation-deadenylation.mRNA多聚腺苷酸化-去腺苷酸化的调控
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Fidelity of protein synthesis does not decline during aging of cultured human fibroblasts.在培养的人类成纤维细胞老化过程中,蛋白质合成的保真度不会下降。
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6
Senescence of cultured human diploid fibroblasts. Are mutations responsible?培养的人二倍体成纤维细胞的衰老。是突变导致的吗?
J Cell Physiol. 1980 May;103(2):209-16. doi: 10.1002/jcp.1041030206.
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On the role of aging in cancer incidence.
J Theor Biol. 1980 Mar 7;83(1):163-73. doi: 10.1016/0022-5193(80)90377-x.
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Status of mitochondria in living human fibroblasts during growth and senescence in vitro: use of the laser dye rhodamine 123.体外培养的人成纤维细胞生长和衰老过程中线粒体的状态:激光染料罗丹明123的应用
J Cell Biol. 1981 Nov;91(2 Pt 1):392-8. doi: 10.1083/jcb.91.2.392.
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Biological significance of liver cell polyploidy: an hypothesis.肝细胞多倍体的生物学意义:一种假说。
J Theor Biol. 1981 Apr 21;89(4):557-71. doi: 10.1016/0022-5193(81)90028-x.
10
Steroid hormone regulation of ovalbumin and conalbumin gene transcription. A model based upon multiple regulatory sites and intermediary proteins.类固醇激素对卵清蛋白和伴清蛋白基因转录的调控。基于多个调控位点和中间蛋白的模型。
J Biol Chem. 1981 Aug 10;256(15):7910-6.