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[端粒替代延长]

[ALT--alternative lengthening of telomere].

作者信息

Wu Xiao-Ming, Tang Wen-Ru, Luo Ying

机构信息

Lab of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650224, China.

出版信息

Yi Chuan. 2009 Dec;31(12):1185-91.

PMID:20042385
Abstract

The maintenance of the length and normal structure of telomeres is highly related to the development of senescence and tumorigenesis. The mechanisms of maintaining telomere are essential for cell growth and the reactivation of these mechanisms is an important step in tumor progression. The mechanism of telomere maintenance might be the reactivation of telomerase. In the case of telomerase deficiency, the mechanisms for maintaining the lengths of telomeres are referred to as alternative lengthening of telomere (ALT). The characteristics of the ALT cells include great heterogeneity of telomere size in individual cells, ALT-associated PML (promyelocytic leukemia) bodies, and evident homologous recombination. The ALT-related proteins and elevated homologous recombination found in ALT cells provide a possible mechanism for the alternative lengthening of telomere. The study of ALT provides a new view of crosstalk between senescence and tumorigenesis.

摘要

端粒长度和正常结构的维持与衰老及肿瘤发生发展密切相关。维持端粒的机制对细胞生长至关重要,而这些机制的重新激活是肿瘤进展的重要步骤。端粒维持机制可能是端粒酶的重新激活。在端粒酶缺乏的情况下,维持端粒长度的机制被称为端粒替代延长(ALT)。ALT细胞的特征包括单个细胞中端粒大小的高度异质性、ALT相关的早幼粒细胞白血病(PML)小体以及明显的同源重组。ALT细胞中发现的ALT相关蛋白和升高的同源重组为端粒替代延长提供了一种可能的机制。对ALT的研究为衰老与肿瘤发生之间的相互作用提供了新的视角。

相似文献

1
[ALT--alternative lengthening of telomere].[端粒替代延长]
Yi Chuan. 2009 Dec;31(12):1185-91.
2
Telomerase-independent telomere length maintenance in the absence of alternative lengthening of telomeres-associated promyelocytic leukemia bodies.在缺乏与端粒延长相关的早幼粒细胞白血病小体的替代延长的情况下,不依赖端粒酶的端粒长度维持。
Cancer Res. 2005 Apr 1;65(7):2722-9. doi: 10.1158/0008-5472.CAN-04-2881.
3
Effects of reconstitution of telomerase activity on telomere maintenance by the alternative lengthening of telomeres (ALT) pathway.端粒酶活性重建对通过端粒替代延长(ALT)途径进行端粒维持的影响。
Hum Mol Genet. 2001 Sep 1;10(18):1953-61. doi: 10.1093/hmg/10.18.1953.
4
Telomere maintenance by telomerase and by recombination can coexist in human cells.端粒酶和重组作用对端粒的维持可在人类细胞中共存。
Hum Mol Genet. 2001 Sep 1;10(18):1945-52. doi: 10.1093/hmg/10.18.1945.
5
PML induces compaction, TRF2 depletion and DNA damage signaling at telomeres and promotes their alternative lengthening.PML在端粒处诱导压缩、TRF2缺失和DNA损伤信号传导,并促进其替代延长。
J Cell Sci. 2015 May 15;128(10):1887-900. doi: 10.1242/jcs.148296. Epub 2015 Apr 23.
6
Coexistence of alternative lengthening of telomeres and telomerase in hTERT-transfected GM847 cells.在转染hTERT的GM847细胞中,端粒替代延长与端粒酶的共存。
Mol Cell Biol. 2001 Jun;21(12):3862-75. doi: 10.1128/MCB.21.12.3862-3875.2001.
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A novel telomere structure in a human alternative lengthening of telomeres cell line.一种人类端粒延长替代细胞系中的新型端粒结构。
Cancer Res. 2005 Apr 1;65(7):2730-7. doi: 10.1158/0008-5472.CAN-04-2888.
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Alternative lengthening of telomeres in mammalian cells.哺乳动物细胞中端粒的替代性延长
Oncogene. 2002 Jan 21;21(4):598-610. doi: 10.1038/sj.onc.1205058.
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Telomere maintenance in Wilms tumors: first evidence for the presence of alternative lengthening of telomeres mechanism.Wilms 瘤中的端粒维持:端粒非经典延长机制存在的初步证据。
Genes Chromosomes Cancer. 2011 Oct;50(10):823-9. doi: 10.1002/gcc.20903. Epub 2011 Jul 18.
10
The telomere-associated homeobox-containing protein TAH1/HMBOX1 participates in telomere maintenance in ALT cells.端粒相关同源盒蛋白 TAH1/HMBOX1 参与 ALT 细胞中端粒的维持。
J Cell Sci. 2013 Sep 1;126(Pt 17):3982-9. doi: 10.1242/jcs.128512. Epub 2013 Jun 26.

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Telomere Maintenance Mechanisms in a Cohort of High-Risk Neuroblastoma Tumors and Its Relation to Genomic Variants in the and Genes.一组高危神经母细胞瘤肿瘤中的端粒维持机制及其与 和 基因中基因组变异的关系。
Cancers (Basel). 2023 Dec 7;15(24):5732. doi: 10.3390/cancers15245732.
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Zscan4 interacts directly with human Rap1 in cancer cells regardless of telomerase status.在癌细胞中,无论端粒酶状态如何,Zscan4都直接与人类Rap1相互作用。
Cancer Biol Ther. 2014 Aug;15(8):1094-105. doi: 10.4161/cbt.29220. Epub 2014 May 19.