ATM基因与AT细胞辐射敏感性的研究进展

史芳; 王芳

史芳 , 王芳

文章导航 > 国际放射医学核医学杂志 > 2007, 31 > 4: (248-250)

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ATM基因与AT细胞辐射敏感性的研究进展

史芳¹,
王芳²

1. 300222 天津, 天津医学高等专科学校医学遗传学教研室;
2. 300020 天津, 天津市血液学研究所血液病医院检测中心
中图分类号: Q345⁺.2

Advances in research on radiosensitivity of AT cells and AT mutated gene

SHI Fang¹,
WANG Fang²

1. Department of Medical Genetics, Tianjin Medical College, Tianjin 300222, China;
2. Department of Test Certer, hutitute of Hematology and Blood Diseases Hospitl, Tianjin 300020, China
CLC number: Q345⁺.2

摘要: 共济失调性毛细血管扩张(AT)是由突变型AT(ATM)基因所引起,其突出特点是AT细胞辐射高敏感性。AT临床症状、ATM基因的定位、结构与功能已基本明确,近年来人们对ATM基因突变与AT细胞辐射敏感性的相关性研究已引起广泛重视,使其成为研究辐射增敏的一个重要的契入点。
- 共济失调性毛细血管扩张 /
- 基因,ATM /
- 辐射耐受性 /
- 基因表达调控
Abstract: Ataxia-telangiectasia(AT) is caused by the mutation of AT(ATM)mutated gene and it is characterized by high radiosensitivity of AT calls. Progress in the research of AT is reviewed in this paper, including the clinical symptoms of this disorder, as well as the localization, structure and function of ATM gene, and summarized the studies on the gene mutation and high radiosensitivity of AT cells in recent years. Further study to ATM gene may provide an important entrance for radiosensitivity-related therapy.
- Ataxia telangiectasia /
- gene, ataxia telangiectasia mutated /
- Rdiation tolerance /
- Gene expression regulation
本作品遵循Signature-Non-Commercial Use 4.0 International (CC BY-NC 4.0)协议

[1]	Chun HH,Gatti RA. Ataxia-telanglectasia,an evolving phenotype.DNA Repair,2004,3(8-9):1187-1196.
[2]	McGowan CH,Russell P. The DNA damage response:sensing and signaling.Cur Open Cell Boil,2004,16(6):629-633.
[3]	Cao JP,Fritz E,Meyn MS. TEL1 from S cerevisiae suppresses chromosome aberrations induced by ionizing radiation in ataxia telangiectasia cells without affecting cell cycle checkpoints.Radiate Environ Biophs,2001,40:309-315.
[4]	Nowak R. Discovery of AT gene sparks biomedical research bonanza.Science,1995,268(5218):1700-1701.
[5]	Eastman A. Cell cycle checkpoints and their impact on anticancer therapeutic strategies.Journal of Cellular Biochemistry,2004,(2):223-231.
[6]	Brew CT,Aronchik I,Hsu JC,et al. Indole-3-carbinol activates the ATM signaling pathway independent of DNA damage to stabilize p53 and induce G1 arrest of human mammary epithelial cells.Int J Cancer,2006,118(4):857-868.
[7]	Eastman A. Cell cycle checkpoints and their impact on anticancer therapeutic strategies.J Cell Biochem,2004,91(2):223-231.
[8]	Prnin D,Bay JO,Uhchammer N,et al. ATM heterozygote cells exhibit intermediate levels of apoptosis in response to atreptonigrin and topside.Eur J Cancer,1999,357:1130-1135.
[9]	O, Driscoll M,Penny A J. The role of double-strand break repair-insightsfrom human genetics.Nature Reviews Genetics,2006,7(1):45-54.
[10]	Enoch T,Norbury C. Cellular responses to DNA damage:cell-cycle checkpoints apoptosis and the roles of p53 and ATM.Trends Biochem Sci,1995,20(10):426-430.
[11]	Gurley KE,Kemp CJ. synthetic lethality between mutation in ATM and DNA-PK(cs) during marine embryogenesis.Curr Biol,2001,11(3):193-194.
[12]	Hong S,Pusapati RV,Powers JT,et al. Oncogenesand the DNA damage responses:M ye and E-F1 engage the ATM signaling pathway to activate p53 and induce apoptosis.Cell Cycle,2006,5(8):801-803.
[13]	Aude D,ChatenetL B,JeanG. Two-stepactivation of ATM by DNA and the M rel 1-Rad50-Nbs1 complex.Nature Struct Mol Biol,2006,13(5):451-457.
[14]	Buscemi G,Perego P,Carenini N,et al. Activation of ATM and Chk2 kinases in relation to the amount of DNA strand breaks.Oncogene,2004,23(46):7691-7700.
[15]	VI t JP,Mustaochi E,Roesclli F. ATM protein is required for radiation induced apoptosis and acts before mitoehondrial collapse.Int J Radiat Biol,2000,76(6):841-851.
[16]	Thompson D,Duedal S,Kirner J,et al. Cancer risksandmor-tality inheterzygous ATM mutation carriers.Natl Cancer Nst,2005,97(11):813-822.
[17]	Turnbull C,Mirugaesu N,Eeles R. Radiotherapy and genetic predis position to breast cancer.Clin Oncol,2006,18(3):257-267.
[18]	Nakai-Murakami C,Shimura M,Kinomoto M,et al. HIV-1 vprindu-ces ATM-dependent cellular signal with enhanced homologous recombination.Oncogene,2007,26(4):477-486

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