[1]贾立立,樊飞跃.Gadd45与基因组稳定性[J].国际放射医学核医学杂志,2009,33(2):105-109.[doi:10.3760/cma.j.issn.1673-4114.2009.02.013]
 JIA Li-li,FAN Fei-yue.Gadd45 and genomic stability[J].International Journal of Radiation Medicine and Nuclear Medicine,2009,33(2):105-109.[doi:10.3760/cma.j.issn.1673-4114.2009.02.013]
点击复制

Gadd45与基因组稳定性(/HTML)
分享到:

《国际放射医学核医学杂志》[ISSN:1673-4114/CN:12-1381/R]

卷:
33
期数:
2009年第2期
页码:
105-109
栏目:
放射生物学
出版日期:
1900-01-01

文章信息/Info

Title:
Gadd45 and genomic stability
作者:
贾立立 樊飞跃
北京协和医学院, 中国医学科学院放射医学研究所生物学研究室, 天津 300192
Author(s):
JIA Li-li FAN Fei-yue
Department of Biology Laboratory, Institute of Radiation Medicine, Chinese Academy of Medical Sciences Peking Union Medical College, Tianjin 300192, China
关键词:
基因Gadd45基因组不稳定性肿瘤
Keywords:
Gene Gadd45Genomic instabilityNeoplasms
DOI:
10.3760/cma.j.issn.1673-4114.2009.02.013
摘要:
Gadd45基因是生长抑制及DNA损伤诱导基因家族中的一员,是电离辐射效应基因之一,在细胞周期调控、DNA损伤修复及细胞凋亡过程中发挥重要作用,这使它成为维持基因组稳定性的重要基因,在肿瘤细胞存活、凋亡信号通路中发挥错综复杂的作用,从而参与肿瘤的发生和发展.
Abstract:
Gadd45 gene is one of growth arrest and DNA damage-inducible(Gadd)family.It’s also a gene induced by ionization radiation.It plays an important role in controlling cell cycle,repairing damaged DNA and in cell apoptosis.This makes it work as an improtant gene in mainteining genomic stability.but more importantly it induces cell apoptosis and is a bridge in the cascade process of apoptosis of tumor cell.At the same time,it takes part in tumorigenesis.

参考文献/References:

[1] Ishikawa K, Ishii H, Saito T. DNA damage-dependent cell cycle checkpoints and genomie stability. DNA Cell Biol, 2006, 25(7):406-411.
[2] Friedberg EC. DNA damage and repair. Nature, 2003,421(6921):436-440.
[3] Kastan MB, Bartek J. Cell-cycle checkpoints and cancer. Nature, 2004, 432(7015):316-323.
[4] Cimprich KA, Cortez D. ATR:an essential regulator of genome integrity. Nat Rev Mol Cell Biol, 2008, 9(8):616-627.
[5] Liu J, Lin A. Role of JNK activation in apoptosis:a double-edged sword. Cell Res, 2005, 15(1):36-42.
[6] Abdollahi A, Lord KA, Hoffman-Liebermann B, et al. Sequence and expression of a cDNA encoding MyD118:a novel myeloid differentiation primary response gene induced by multiple cytokines. Oncogene, 1991, 6(1):165-167.
[7] Vairapandi M, Balliet AG, Hoffman B, et al. GADD45b and GADD45g are cdc2/cyclinB1 kinase inhibitors with a role in S and GJM cell cycle checkpoints induced by genotoxic stress. J Cell Physiol, 2002, 192(3):327-338.
[8] Yoo J, Ghiassi M, Jirmanova L, et al. Transforming growth factorbeta-induced apoptosis is mediated by Smad-dependent expression of GADD45b through p38 activation. J Biol Chem, 2003, 278(44):43001-43007.
[9] Jung HJ, Kim EH, Mun JY, et al. Base excision DNA repair defect in Gadd45a-deficient cells. Oncogene, 2007, 26(54):7517-7525.
[10] Desjardins S, Ouellette G, Labile Y, et al. Analysis of GADD45A sequence variations in French Canadian families with high risk of breast cancer. J Hum Genet, 2008, 53(6):490-498.
[11] Zhan Q. Gadd45a, a p53 and BRCAl-regulated stress protein, in cellular response to DNA damage. Mutat Res, 2005, 569(1-2):133-143.
[12] Wang XW, Zhan Q, Coursen JD, et al. GADD45 induction of a G2/M cell cycle checkpoint. Proc Natl Acad Sci USA, 1999, 96(7):3706-3711.
[13] Han C, Demetris AJ, Michalopoulos GK, et al. PPARgamma ligands inhibit cholangiocarcinoma cell growth through p53-dependent GADD45 and p21 pathway. Hepatology, 2003, 38(1):167-177.
[14] Smith GB, Mocarski ES. Contribution of GADD45 family members to cell death suppression by cellular Bcl-xL and cytomegalovirus vMIA. J Virol, 2005, 79(23):14923-14932.
[15] Liebermann DA, Hoffman B. Gadd45 in the response of hematopoietic cells to genotoxic stress. Blood Cells Mol Dis, 2007, 39(3):329-335.
[16] Ying J, Srivastava G, Hsieh WS, et al. The stress-responsive gene GADD45G is a functional tumor suppressor, with its response to environmental stresses frequently disrupted epigenetically in muhiple tumors. Clin Cancer Res, 2005, 11(18):6442-6449.
[17] Tront JS, Hoffman B, Liebermann DA. Gadd45a suppresses Rasdriven mammary tumorigenesis by activation of c-Jun NH2-terminal kinase and p38 stress signaling resulting in apoptosis and senescence. Cancer Res, 2006, 66(17):8448-8454.
[18] Candal E, Thermes V, Joly JS, et al. Medaka as a model system for the characterisation of cell cycle regulators:a functional analysis of Ol-Gadd45gamma during early embryogenesis. Mech Dev, 2004, 121(7-8):945-958.
[19] Maeda T, Espino RA, Chomey EG, et al. Loss of p21WAF1/Cipl in Gadd45-deficient keratinocytes restores DNA repair capacity. Carcinogenesis, 2005, 26(10):1804-1810.
[20] Vairapandi M, Balliet AG, Fornace AJ Jr, et al. The differentiation primary response gene MyD118, related to GADIMS, encodes for a nuclear protein which interacts with PCNA and p21WAFI/CIP1. Oncogene, 1996, 12(12):2579-2594.
[21] Gupta SK, Gupta M, Hoffman B, et al. Hematopoietic cells from gadd45a-deficient and gadd45b-defieient mice exhibit impaired stress responses to acute stimulation with cytokines, myeloablation and inflammation. Oneogene, 2006, 25(40):5537-5546.
[22] Barreto G, Schafer A, Marhold J, et al. Gadd45a promotes epigenetic gene activation by repair-mediated DNA demethylation. Nature, 2007, 445(7128):671-675.
[23] Bulavin DV, Kovalsky O, Hollander MC, et al. Loss of oncogenic H-ras-induced cell cycle arrest and p38 mitogen activated protein kinase activation by disruption of Gadd45a. Mol Cell Biol, 2003, 23(11):3859-3871.
[24] Hollander MC, Fornace AJ Jr. Genomic instability, centrosome amplification, cell cycle checkpoints and Gadd45a, Oncogene, 2002, 21(40):6228-6233.
[25] Wang X, Wang RH, Li W, et al. Genetic interactions between Brcal and Gadd45a in centrosome duplication, genetic stability, and neural tube closure. J Biol Chem, 2004, 279(28):29606-29614.
[26] Hollander MC, Philburn RT, Patterson AD, et al. Genomic instability in Gadd45a-/-cells is coupled with S-phase checkpoint defects. Cell Cycle, 2005, 4(5):704-709.
[27] Bishop A J, Hollander MC, Kosaras B, et al. Atm-, p53-, and Gadd45a-deficient mice show an increased frequency of homologous recombination at different stages during development. Cancer Res, 2003, 63(17):5335-5343.
[28] Tront JS, Hoffman B, Liebermann DA. Gadd45a suppresses Rasdriven mammary tumorigenesis by activation of c-Jun NH2-terminal kinase and p38 stress signaling resulting in apoptosis and senescence. Cancer Res, 2006, 66(17):8448-8454.
[29] Lundberg AS, Hahn WC, Gupta P, et al. Genes involved in senescence and immortalization. Curr Opin Cell Biol, 2000, 12(6):705-709.

相似文献/References:

[1]路璐,李德冠,张俊伶,等.RNA干扰沉默p16基因对小鼠胚胎成纤维细胞衰老的影响[J].国际放射医学核医学杂志,2014,38(5):281.[doi:10.3760/cma.j.issn.1673-4114.2014.05.001]
 Lu Lu,Li De-guan,Zhang Jun-ling,et al.Application of RNA interference vector targeting mouse p16 gene in γ-irradiation-induced mouse embryonic fibroblast[J].International Journal of Radiation Medicine and Nuclear Medicine,2014,38(2):281.[doi:10.3760/cma.j.issn.1673-4114.2014.05.001]
[2]王芹,王敬敏,徐畅,等.Ad-Rb94联合照射对体外人大肠癌细胞的抑瘤作用[J].国际放射医学核医学杂志,2014,38(6):351.[doi:10.3760/cma.j.issn.1673-4114.2014.06.001]
 Wang Qin,Wang Jing-min,Xu Chang,et al.The effect of Ad-Rb94 combined with radiation on inhibiting the growth of human colorectal cancer cells in vitro[J].International Journal of Radiation Medicine and Nuclear Medicine,2014,38(2):351.[doi:10.3760/cma.j.issn.1673-4114.2014.06.001]
[3]李敏,孟庆慧,胡旭东,等.B细胞易位基因2的表达水平对肿瘤细胞放射敏感性的影响[J].国际放射医学核医学杂志,2013,37(3):129.[doi:10.3760/cma.j.issn.1673-4114.2013.03.001]
 LI Ming,MENG Qing-hui,HU Xu-dong,et al.Effect of B-cell translocation gene 2 alteration on radiosensitivity of cancer cells[J].International Journal of Radiation Medicine and Nuclear Medicine,2013,37(2):129.[doi:10.3760/cma.j.issn.1673-4114.2013.03.001]
[4]王芹,刘晓秋,李进,等.白细胞介素21基因联合不同剂量γ射线照射对乳腺癌细胞生长的影响[J].国际放射医学核医学杂志,2012,36(2):94.[doi:10.3760/cma.j.issn.1673-4114.2012.02.009]
 WANG Qin,LIU Xiao-qiu,LI Jin,et al.Effects of interleukin-21 gene combined with different doses of γ-ray radiation on growth of breast carcinoma cells[J].International Journal of Radiation Medicine and Nuclear Medicine,2012,36(2):94.[doi:10.3760/cma.j.issn.1673-4114.2012.02.009]
[5]李继涛,何明远,袁德晓,等.p53调控的能量代谢对辐射效应的影响[J].国际放射医学核医学杂志,2012,36(6):380.[doi:10.3760/cma.j.issn.1673-4114.2012.06.014]
 LI Ji-tao,HE Ming-yuan,YUAN De-xiao,et al.Influence of p53-regulated energy metabolism in radiation effects[J].International Journal of Radiation Medicine and Nuclear Medicine,2012,36(2):380.[doi:10.3760/cma.j.issn.1673-4114.2012.06.014]
[6]吴涛,安锐.分子影像报告基因系统的研究进展[J].国际放射医学核医学杂志,2010,34(4):198.[doi:10.3760/cma.j.issn.1673-4114.2010.04.002]
 WU Tao,AN Rui.Advances in study of molecular imaging reporter gene systems[J].International Journal of Radiation Medicine and Nuclear Medicine,2010,34(2):198.[doi:10.3760/cma.j.issn.1673-4114.2010.04.002]
[7]周翔,尹红燕,张一帆.报告基因显像监测干细胞治疗的研究进展[J].国际放射医学核医学杂志,2010,34(5):262.[doi:10.3760/cma.j.issn.1673-4114.2010.05.002]
 ZHOU Xiang,YIN Hong-yan,ZHA NG Yi-fan.Advances of reporter gene monitoring stem cell therapy[J].International Journal of Radiation Medicine and Nuclear Medicine,2010,34(2):262.[doi:10.3760/cma.j.issn.1673-4114.2010.05.002]
[8]裴之俊,张永学.报告基因显像监测干细胞治疗的研究进展[J].国际放射医学核医学杂志,2010,34(2):73.[doi:10.3760/cma.j.issn.1673-4114.2010.02.002]
 PEI Zhi-jun,ZHANG Yong-xue.Advances of reporter gene imaging monitoring stem cell therapy[J].International Journal of Radiation Medicine and Nuclear Medicine,2010,34(2):73.[doi:10.3760/cma.j.issn.1673-4114.2010.02.002]
[9]陈凤华,李进,谭志军,等.Ad-Rb94联合γ射线照射对食管癌细胞生长的影响[J].国际放射医学核医学杂志,2010,34(2):119.[doi:10.3760/cma.j.issn.1673-4114.2010.02.017]
 CHEN Feng-hua,LI Jin,TAN Zhi-jun,et al.Effects of recombinant adenovirus mediated retinoblastoma gene 94 combined with γ-ray on growth of esophageal carcinoma cells[J].International Journal of Radiation Medicine and Nuclear Medicine,2010,34(2):119.[doi:10.3760/cma.j.issn.1673-4114.2010.02.017]
[10]王洗,刘强.脑胶质瘤辐射敏感性相关基因的研究进展[J].国际放射医学核医学杂志,2008,32(5):311.
 WANG Xi,LIU Qiang.The progress of radiosensitive genes of human brain glioma[J].International Journal of Radiation Medicine and Nuclear Medicine,2008,32(2):311.

备注/Memo

备注/Memo:
收稿日期:2008-11-30。
通讯作者:樊飞跃(E-mail:faithyfan@yahoo.com)
更新日期/Last Update: 1900-01-01