Crosstalk of reactive oxygen species and NF-κB signaling

被引:2088
作者
Morgan, Michael J. [1 ]
Liu, Zheng-gang [1 ]
机构
[1] NCI, Cell & Canc Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
reactive oxygen species (ROS); NF-kappa B; oxidative stress; antioxidants; TUMOR-NECROSIS-FACTOR; MANGANESE SUPEROXIDE-DISMUTASE; DNA-BINDING ACTIVITY; HYDROGEN-PEROXIDE FORMATION; TERMINAL KINASE ACTIVATION; EARLY EMBRYONIC LETHALITY; PROTEIN-TYROSINE KINASE; ALPHA-INDUCED APOPTOSIS; NITRIC-OXIDE SYNTHASE; INDUCED CELL-DEATH;
D O I
10.1038/cr.2010.178
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
NF-kappa B proteins are a family of transcription factors that are of central importance in inflammation and immunity. NF-kappa B also plays important roles in other processes, including development, cell growth and survival, and proliferation, and is involved in many pathological conditions. Reactive Oxygen Species (ROS) are created by a variety of cellular processes as part of cellular signaling events. While certain NF-kappa B-regulated genes play a major role in regulating the amount of ROS in the cell, ROS have various inhibitory or stimulatory roles in NF-kappa B signaling. Here we review the regulation of ROS levels by NF-kappa B targets and various ways in which ROS have been proposed to impact NF-kappa B signaling pathways.
引用
收藏
页码:103 / 115
页数:13
相关论文
共 164 条
[1]   Determination of interleukin-4-responsive region in the human cytochrome P450 2E1 gene promoter [J].
Abdel-Razzak, Z ;
Garlatti, M ;
Aggerbeck, M ;
Barouki, R .
BIOCHEMICAL PHARMACOLOGY, 2004, 68 (07) :1371-1381
[2]   Biochemical and cellular toxicology of peroxynitrite: implications in cell death and autoimmune phenomenon [J].
Ahmad, Rizwan ;
Rasheed, Zafar ;
Ahsan, Haseeb .
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY, 2009, 31 (03) :388-396
[3]   Genetic deletion of NAD(P)H:: Quinone oxidoreductase 1 abrogates activation of nuclear factor-κB, IκBα kinase, c-Jun N-terminal kinase, Akt, p38, and p44/42 mitogen-activated protein kinases and potentiates apoptosis [J].
Ahn, Kwang Seok ;
Sethi, Gautam ;
Jain, Abhinav K. ;
Jaiswal, Anil K. ;
Aggarwal, Bharat B. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (29) :19798-19808
[4]   A new APE1/Ref-1-dependent pathway leading to reduction of NF-κB and AP-1, and activation of their DNA-binding activity [J].
Ando, Kozue ;
Hirao, Satoshi ;
Kabe, Yasuaki ;
Ogura, Yuji ;
Sato, Iwao ;
Yamaguchi, Yuki ;
Wada, Tadashi ;
Handa, Hiroshi .
NUCLEIC ACIDS RESEARCH, 2008, 36 (13) :4327-4336
[5]   NF-κB regulates phagocytic NADPH oxidase by inducing the expression of gp91phox [J].
Anrather, J ;
Racchumi, G ;
Iadecola, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (09) :5657-5667
[6]   THE TRANSCRIPTIONAL REGULATION OF HUMAN ARACHIDONATE 12-LIPOXYGENASE GENE BY NF-KAPPA-B/REL [J].
ARAKAWA, T ;
NAKAMURA, M ;
YOSHIMOTO, T ;
YAMAMOTO, S .
FEBS LETTERS, 1995, 363 (1-2) :105-110
[7]   Functions of NF-κB1 and NF-κB2 in immune cell biology [J].
Beinke, S ;
Ley, SC .
BIOCHEMICAL JOURNAL, 2004, 382 :393-409
[8]   Involvement of regulatory and catalytic subunits of phosphoinositide 3-kinase in NF-κB activation [J].
Béraud, C ;
Henzel, WJ ;
Baeuerle, PA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (02) :429-434
[9]   TAK1 is recruited to the tumor necrosis factor-α (TNF-α) receptor 1 complex in a receptor-interacting protein (RIP)-dependent manner and cooperates with MEKK3 leading to NF-κB activation [J].
Blonska, M ;
Shambharkar, PB ;
Kobayashi, M ;
Zhang, DY ;
Sakurai, H ;
Su, B ;
Lin, X .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (52) :43056-43063
[10]   The two NF-κB activation pathways and their role in innate and adaptive immunity [J].
Bonizzi, G ;
Karin, M .
TRENDS IN IMMUNOLOGY, 2004, 25 (06) :280-288