脑组织对DNA双链断裂的反应

董晓荣; 伍钢

脑组织对DNA双链断裂的反应

董晓荣 , 伍钢

文章导航 > 国际放射医学核医学杂志 > 2008, 32 > 1: (51-54)

引用本文:

Citation:

脑组织对DNA双链断裂的反应

董晓荣,
伍钢^,

430023 武汉, 华中科技大学同济医学院附属协和医院肿瘤中心

通讯作者: 伍钢, wugangzr@yahoo.com.cn

中图分类号: Q691.9

The response of the brain tissue to DNA double strand breaks

DONG Xiao-rong,
WU Gang^,

Cancer Center, Wuhan Union Hospital, Huazhong University of Science and Technology, Wuhan 430023, China

Corresponding author: WU Gang, wugangzr@yahoo.com.cn

CLC number: Q691.9

摘要: DNA双链断裂是电离辐射引起的最严重DNA损伤形式,脑组织对DNA损伤的反应与其发展程度密切相关,脑组织中增殖细胞主要是通过同源重组进行修复,而分化细胞则通过非同源末端联接修复。DNA双链断裂信号通路相关因子的缺陷会导致一系列的有神经病理表现的人类遗传病。重点讨论电离辐射触发脑细胞DNA双链断裂后,信号转导相关因子和与相关因子导致的神经系统人类遗传疾病。
- 辐射损伤 /
- 信号传导 /
- DNA损伤 /
- DNA修复 /
- 脑
Abstract: Double-strand breaks (DSB) are the most deleterious form of DNA damage after ionizing radiation, the response of the brain tissue to DNA damage is related to the developmental dynamics of this system. Homology recombination is particularly important for proliferating cells, while non-homologous end joining is critical for differentiating cells. Defects in the related factors to DNA damage pathway underpin many human genopathy with neuropathology. Reviewed the signal conduction system involved in the DNA DSB response and human neuropathology genopathy related to DNA DSB factors deficiencies in the brain cells.
- Radiation injuries /
- Signal transduetion /
- DNA damage /
- DNA repair /
- Brain
本作品遵循Signature-Non-Commercial Use 4.0 International (CC BY-NC 4.0)协议

[1]	Sedelnikova OA, Pilch DR, Redon C, et al. Histone H2AX in DNA damage and repair[J]. Cancer Biol Ther, 2003, 2(3):233-235.
[2]	Fernandez-Capetillo O, Lee A, Nussenzweig M, et al. H2AX:the histone guardian of the genome[J]. DNA Repair (Amst), 2004, 3(8-9):959-967.
[3]	Rothkamm K, Lobrich M. Evidence for a lack of DNA doublestrand break repair in human cells exposed to very low X-ray doses[J]. Proc Natl Acad Sci USA, 2003, 100(9):5057-5062.
[4]	Stiff T, O'Driscoll M, Rief N, et al. ATM and DNA-PK function redundantly to phosphorylate H2AX following exposure to ionising radiation[J]. Cancer Res, 2004, 64(7):2390-2396.
[5]	Stucki M, Clapperton JA, Mohammad D, et al. MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks[J]. Cell, 2005, 123(7):1213-1226.
[6]	Lou Z, Minter-Dykhouse K, Franco S, et al. MDC1 maintains genomic stability by participating in the amplification of ATM-dependent DNA damage signals[J]. Mol Cell, 2006, 21(2):187-200.
[7]	Lavin MF, Birrell G, Chen P, et al. ATM signaling and genomic stability in response to DNA damage[J]. Mutat Res, 2005, 569(1-2):123-132.
[8]	Kurz EU, Lees-Miller SP. DNA damage-induced activation of ATM and ATM-dependent signaling pathways[J]. DNA Repair (Amst), 2004, 3(8-9):889-900.
[9]	Lee JH, Paull TT. Direct activation of the ATM protein kinase by the Mre11/Rad50/Nbs1 complex[J]. Science, 2004, 304(5667):93-96.
[10]	Difilippantonio S, Celeste A, Femandez-Capetillo O, et al. Role of Nbs1 in the activation of the Atm kinase revealed in humanized mouse models[J]. Nat Cell Biol, 2005, 7(7):675-685.
[11]	Riballo E, Kuhne M, Rief N, et al. A pathway of double-strand break rejoining dependent upon ATM, Artemis and proteins locating to γ-H2AX foci[J]. Mol Cell, 2004, 16(5):715-724.
[12]	Abner CW, McKinnon PJ. The DNA double-strand break response in the nervous system[J]. DNA Repair (Amst), 2004, 3(8-9):1141-1147.
[13]	O'Driscoll M, Jeggo PA. The role of double-strand break repair:insights from human genetics[J]. Nat Rev Genet, 2006, 7(1):45-54.
[14]	Orii KE, Lee Y, Kondo N, et al. Selective utilization of nonhomologous end-joining and homologous recombination DNA repair pathways during nervous system development[J]. Proc Natl Acad Sci USA, 2006, 103(26):10017-10022.
[15]	McKinnon PJ. ATM and ataxia telangiectasia[J]. EMBO Rep, 2004, 5(8):772-776.
[16]	Taylor AM, Groom A, Byrd PJ. Ataxia-telangiectasia-like disorder (ATLD):its clinical presentation and molecular basis[J]. DNA Repair (Amst), 2004, 3(8-9):1219-1225.
[17]	Digweed M, Sperling K. Nijmegen breakage syndrome:clinical manifestation of defective response to DNA double-strand breaks[J]. DNA Repair(Amst), 2004, 3(8-9):1207-1217.

[1]	高宇 , 徐畅 , 刘强 . EGFR和NRF2对电离辐射导致的DNA损伤修复的影响. 国际放射医学核医学杂志, 2023, 47(4): 211-219. doi: 10.3760/cma.j.cn121381-202303015-00294
[2]	程晋 , 邹仲敏 . DNA损伤修复及细胞周期检控点激活的研究进展. 国际放射医学核医学杂志, 2009, 33(6): 360-364. doi: 10.3760/cma.j.issn.1673-4114.2009.06.014
[3]	丘冠英 . DNA辐射损伤研究:热点与新进展. 国际放射医学核医学杂志, 2002, 26(4): 145-147.
[4]	张焕腾 , 孙毓筱 , 徐畅 . 泛素化修饰和SUMO化修饰在电离辐射诱导的DNA损伤修复中的作用机制. 国际放射医学核医学杂志, 2024, 48(2): 130-136. doi: 10.3760/cma.j.cn121381-202308031-00389
[5]	牛津梁 . DNA损伤修复能力对GPA基因突变频率的影响及其检测方法. 国际放射医学核医学杂志, 2001, 25(6): 279-282.
[6]	郭阳 . DNA链间交联的修复与辐射敏感性. 国际放射医学核医学杂志, 2007, 31(6): 371-372,376.
[7]	由莉 , 赵永成 . γ-H2AX分析及其在监测电离辐射所致DNA双链断裂中的应用前景. 国际放射医学核医学杂志, 2006, 30(1): 50-52.
[8]	李平 , 宗天舟 , 季晓芹 , 陆雪官 . CD133⁺ U87人脑胶质瘤干细胞放射敏感性和DNA双链断裂损伤修复的实验研究. 国际放射医学核医学杂志, 2013, 37(3): 153-159. doi: 10.3760/cma.j.issn.1673-4114.2013.03.007
[9]	王芹 , 刘晓秋 , 刘强 , 李进 , 樊飞跃 . DNA双链断裂修复途径中重要的修复蛋白. 国际放射医学核医学杂志, 2013, 37(1): 34-37. doi: 10.3760/cma.j.issn.1673-4114.2013.01.010
[10]	郑秀龙 . DNA分子水平的放射效应研究. 国际放射医学核医学杂志, 1996, 20(1): 32-35.
[11]	林曰增 . 脑放射损伤的影像学研究进展. 国际放射医学核医学杂志, 2000, 24(4): 148-151.

点击查看大图

计量

文章访问数: 1408
HTML全文浏览量: 117
PDF下载量: 2

脑组织对DNA双链断裂的反应

董晓荣
伍钢^,

通讯作者: 伍钢, wugangzr@yahoo.com.cn

430023 武汉, 华中科技大学同济医学院附属协和医院肿瘤中心

收稿日期: 2007-07-26

关键词:

摘要: DNA双链断裂是电离辐射引起的最严重DNA损伤形式,脑组织对DNA损伤的反应与其发展程度密切相关,脑组织中增殖细胞主要是通过同源重组进行修复,而分化细胞则通过非同源末端联接修复。DNA双链断裂信号通路相关因子的缺陷会导致一系列的有神经病理表现的人类遗传病。重点讨论电离辐射触发脑细胞DNA双链断裂后,信号转导相关因子和与相关因子导致的神经系统人类遗传疾病。