NF-κB不同二聚体的活化与辐射诱导凋亡的关系

何淑杰; 刘树铮

何淑杰 , 刘树铮

文章导航 > 国际放射医学核医学杂志 > 2001, 25 > 2: (74-77)

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NF-κB不同二聚体的活化与辐射诱导凋亡的关系

130021 长春, 卫生部放射生物学重点实验室

作者简介: 何淑杰(1967-),女,吉林农安人,白求恩医科大学放射生物室博士,现在新西兰做博士后研究工作。;刘树铮(1925-),男,湖南长沙人,白求恩医科大学卫生部放射生物重点实验室教授,博士生导师,主要从事低水平辐射生物效应研究。;

中图分类号: R818.03

The relation between activation of different dimers of NF-κB and radiation-induced apoptosis

Radiobiology Research Unit, Ministry of Health, PRC, Changchun 130021, China
CLC number: R818.03

摘要: 转录因子κ基因结合核因子(NF-κB)一直被看作是细胞的存活因子,对辐射诱导的细胞凋亡起强烈的抵抗作用。然而,近来的研究逐渐表明,NF-κB不同亚基的组合可能有着不同、甚至完全相反的作用。对这方面课题的深入研究,无疑对理解中、高剂量辐射免疫抑制效应的机制可提供有意义的理论依据,并对临床肿瘤的放疗将提供新的有价值的资料。
- NF-κB /
- 辐射 /
- 细胞凋亡
Abstract: NF-κB used to be considered as a surviving factor, conferring vigorous resistance to cells against radiation-induced apoptosis. However, recent research gradually disclosed that combination of different subunits of NF-κB may have different, even opposite effects. Further investigation in more depth would undoubtedly provide theoretical basis for the understanding of the mechanism of the depressive effect of medium to high doses of radiation on immunity and valuable new information for radiotherapy of clinical tumors.
- NF-κB /
- radiation /
- apoptosis
本作品遵循Signature-Non-Commercial Use 4.0 International (CC BY-NC 4.0)协议

[1]	Maniatis T.A ubiquitin ligase complex essential for the NF-κB,Wnt/Wingless and Hedgehog signaling pathways[J].Genes Dev,1999,13:505-510.
[2]	Ghosh S,May M J,Kopp EB.NF-κB and Rel proteins:evolutionarily conserved mediators of immune response[J].Ann Rev Immunol,1998,16:225-260.
[3]	He SJ,Jin SZ,Liu SZ.Effect of whole-body X-irradiation on NF-κB activity in immune organs[J].J Radiat Res Radiat Proc,2000,18(4):278-283.
[4]	Miyamoto S,Verma IM.Rel/NF-κB/IκB story[J].Adv Cancer Res,1995,66:255-292.
[5]	Attar RM,Caamano J,Carraseo D,et al.Genetic approaches to study Rel/NF-κB/IκB function[J].Semin Cancer Biol,1997,8:93-101.
[6]	Roulston A,Lin R,Beauparlant P,et al.Regalation of human immunodeficiency virus I and cytokine gene expression in myeloid cells by NF-κB/Rel transcription factors[J].Microbiol Rev,1995,59:481-505.
[7]	Bex F,Gaynor RB.Regulation of gene expression by HTLV-I Tax protein[J].Methods,1998,16:83-94.
[8]	Sha WC,Liou HC,Tuomanen E,et al.Targeted disruption of the p50 subunit of NF-kappaB leads to multifocal defects in immune responses[J].Cell,1995,80:321-330.
[9]	Iotsova V,Caamano J,Loy J,et al.Osteoporosis inmice lacking NF-κB1 and NF-κB2[J].Nat Med,1997,3:1285-1289.
[10]	Baichwal VR,Baeuerle PA.Activate NF-κB or die?[J]Curr Biol,1997,7:94-96.
[11]	Sonenshein GE.NF-κB transcription factors and the control of apoptosis[J] Semin Cancer Biol,1997,8:113-119.
[12]	Beg AA,Sha WC,Bronson RT,et al.Embrionic lethality and liver degeneration inmmice lacking the RelA component of NF-κB[J].Nature,1995,376:167-169.
[13]	Beg AA,Baltimone D.An essential role for NF-κB in preventing TNF-α-induced cell death[J].Science,1996,274:782-784.
[14]	Wang CC,Mayo MW,Baldwin Jr AS.TNF-and cancer therapy-induced apoptosis potentiation by inhibition of NF-κB[J].Science,1996,274:784-787.
[15]	Grimm S,Bauer M,Baeuerle PA,et al.Bcl-2 down-regulation the activity of transcription factor NF-κB induced upon apoptosis[J].J Cell Biol,1996,34:13-23.
[16]	Jung M,Zhang Y,Lee S,et al.Correction of radiation sensitivity in atxia telengiectasis by a truncated IκBα[J].Science,1995,268:1619-1621.
[17]	Abbadie C,Kabrun N,Bouali F,et al.High levels of c-Rel expression are associated with progammed cell death in developing avian embryo and in bone marrow cells in vitro[J].Cell,1993,75:899-912.
[18]	Bash J,Zong WX,Gelinas C.c-Rel arrests the proliferation of HeLa cells and affects critical regulators of the G1/S-phase transition[J].Mol Cell Biol,1997,17:6526-6536.
[19]	Zong WX,Farrell M,Bash J,et al.v-Rel prevents apoptosis in transformed lymphoid cells and blocks TNF-α-induced cell death[J].Oncogene,1997,15:971-980.
[20]	Tsunta L,Lee HJ,Masuda ES,et al.Cyclic AMP inhibits expression of the IL-2 gene through the nuclear factor of activated T cells (NF-AT) site and transfection of NF-AT cDNAs abrogates the sensitivity of EL-4 cells to cyclic AMP[J].J Immunol,1995,154:5255.
[21]	Zwollo P,Rao S,Wallin JJ,et al.The transcription factor NF-κB/p50 interacts with the blk gene during B cell activation[J].J Biol Chem,1998,273:18647.
[22]	Kang SM,Tran AAC,Grill M.NE-κB subunit regulation in non-transformed CD4⁺T lymphocytes[J].Science,1992,256:1452-1456.
[23]	Wang CY,Cusack JC,Liu R,et al.Control of inducible chemoresistance:Enhanced anti-tumor therapy through increased apoptosis by inhibition of NF-κB[J].Nature Med,1999,5:412-417.
[24]	Chen D,Rothenberg EV.Molecular basis for developmental changes in IL-2 gene inducibility[J].Mol Cell Biol,1993,133:228-237.
[25]	Liu SZ,Zhang YC,Mu Y,et al.Thymocyte apoptosis in response to low dose radiation[J].Mutat Res,1996,358:185-191.
[26]	Liu SZ.Multilevel mechanisms of stimulatory effect of low dose radiation on immunity[A].Sugahara T,Sagan L A and Aoyama T.Low dose irradiation and biological defense mechanisms[C].Elsevier Science Publishers,1992,225-232.
[27]	Prasad AV,Mohan N,Chandrasekar B,et al.Activation of nuclear factor kappa B in human lymphoblastoid cells by low dose ionizing radiation[J].Radia Res,1994,138:367-372.
[28]	Rice NR,Mackichan ML,Israel A.The precursor of NF-κB p50 has IκB-like functions[J].Cell,1992,78:773-785.
[29]	Belich MP,Salmer A,Johnston LH,et al.TPL-2 kinase regulates the proteolytic processing of the human NF-κB1 precursor[J].Cene,1999,397:363-368.

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NF-κB不同二聚体的活化与辐射诱导凋亡的关系

作者简介:何淑杰(1967-),女,吉林农安人,白求恩医科大学放射生物室博士,现在新西兰做博士后研究工作。;刘树铮(1925-),男,湖南长沙人,白求恩医科大学卫生部放射生物重点实验室教授,博士生导师,主要从事低水平辐射生物效应研究。

130021 长春, 卫生部放射生物学重点实验室

收稿日期: 2000-12-05

关键词:

NF-κB /
辐射 /
细胞凋亡

摘要: 转录因子κ基因结合核因子(NF-κB)一直被看作是细胞的存活因子,对辐射诱导的细胞凋亡起强烈的抵抗作用。然而,近来的研究逐渐表明,NF-κB不同亚基的组合可能有着不同、甚至完全相反的作用。对这方面课题的深入研究,无疑对理解中、高剂量辐射免疫抑制效应的机制可提供有意义的理论依据,并对临床肿瘤的放疗将提供新的有价值的资料。