Redox control of cell fate by MAP kinase: physiological roles of ASK1-MAP kinase pathway in stress signaling

Matsuzawa, Atsushi; Ichijo, Hidenori

doi:10.1016/j.bbagen.2007.12.011

Cited by 443 publications

(353 citation statements)

References 92 publications

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“…The formation of this complex is dependent on the presence of a reduced form of an intramolecular disulfide bridge between two cysteine residues of thioredoxin. Oxidation of thioredoxin by ROS causes the dissociation of ASK-1 from thioredoxin, resulting in the activation of ASK1 by oligomerization, interaction with TNF receptor-associated factor-2/6, and threonine autophosphorylation (103). It has been shown that ROS production from Nox4 can activate p38 via the activation of ASK-1 (24).…”

Section: P38mentioning

confidence: 99%

“…p38 is a member of the MAPK family of signal transduction kinases, which can be activated in a sequential order (mitogen-activated or extracellular signal-regulated kinase kinase [MEKK]-MAPK kinase 3/6 [MKK3/6]-p38) after exposure to stress (83). In addition, oxidative stress can also activate p38 via the activation of apoptosis signal-regulating kinase 1 (ASK1) (103) and/or inactivation of protein tyrosine phosphatases (PTPs), such as MAPK phosphatases (77,128). Normally, ASK-1 forms an inactive complex with the repressor protein thioredoxin in a cell.…”

Section: P38mentioning

confidence: 99%

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Hematopoietic Stem Cell Injury Induced by Ionizing Radiation

Shao

Luo

Zhou

2014

Antioxidants & Redox Signaling

258

218

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Significance: Exposure to ionizing radiation (IR) as the result of nuclear accidents or terrorist attacks is a significant threat and a major medical concern. Hematopoietic stem cell (HSC) injury is the primary cause of death after accidental or intentional exposure to a moderate or high dose of IR. Protecting HSCs from IR should be a primary goal in the development of novel medical countermeasures against radiation. Recent Advances: Significant progress has been made in our understanding of the mechanisms by which IR causes HSC damage. The mechanisms include (i) induction of HSC apoptosis via the p53-Puma pathway; (ii) promotion of HSC differentiation via the activation of the G-CSF/Stat3/BATF-dependent differentiation checkpoint; (iii) induction of HSC senescence via the ROS-p38 pathway; and (iv) damage to the HSC niche. Critical Issues: Induction of apoptosis in HSCs and hematopoietic progenitor cells is primarily responsible for IR-induced acute bone marrow (BM) injury. Long-term BM suppression caused by IR is mainly attributable to the induction of HSC senescence. However, the promotion of HSC differentiation and damage to the HSC niche can contribute to both the acute and long-term effects of IR on the hematopoietic system. Future Directions: In this review, we have summarized a number of recent findings that provide new insights into the mechanisms whereby IR damages HSCs. These findings will provide new opportunities for developing a mechanism-based strategy to prevent and/or mitigate IR-induced BM suppression.

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Section: P38mentioning

confidence: 99%

Section: P38mentioning

confidence: 99%

Hematopoietic Stem Cell Injury Induced by Ionizing Radiation

Shao

Luo

Zhou

2014

Antioxidants & Redox Signaling

258

218

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“…ROS also alters the expression of the p53 suppressor gene that is key in apoptosis. Thus, oxidative stress caused by changes in gene expression, cell proliferation, apoptosis, and angiogenesis plays a significant role in tumor initiation and progression (Matsuzawa and Ichijo, 2008;Nguyen et al, 2009;Wiemer, 2011;Barrera, 2012).…”

Section: Oxidative Stress and Cancermentioning

confidence: 99%

Roles of Oxidative Stress in the Development and Progression of Breast Cancer

Nourazarian¹,

Kangari²,

Salmaninejad³

2014

Asian Pacific Journal of Cancer Prevention

150

108

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Oxidative stress is caused by an imbalance in the redox status of the body. In such a state, increase of free radicals in the body can lead to tissue damage. One of the most important species of free radicals is reactive oxygen species (ROS) produced by various metabolic pathways, including aerobic metabolism in the mitochondrial respiratory chain. It plays a critical role in the initiation and progression of various types of cancers. ROS affects different signaling pathways, including growth factors and mitogenic pathways, and controls many cellular processes, including cell proliferation, and thus stimulates the uncontrolled growth of cells which encourages the development of tumors and begins the process of carcinogenesis. Increased oxidative stress caused by reactive species can reduce the body's antioxidant defense against angiogenesis and metastasis in cancer cells. These processes are main factors in the development of cancer. Bimolecular reactions cause free radicals in which create such compounds as malondialdehyde (MDA) and hydroxyguanosine. These substances can be used as indicators of cancer. In this review, free radicals as oxidizing agents, antioxidants as the immune system, and the role of oxidative stress in cancer, particularly breast cancer, have been investigated in the hope that better identification of the factors involved in the occurrence and spread of cancer will improve the identification of treatment goals.

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“…Although our data here clearly show that oxidation inactivates MAP2Ks, paradoxically, some reports showed that oxidation could activate various MAPKs (29,36), whereas others claimed that oxidation had minimal effect on the activity of selected MAPKs (37,38). A survey of the literature suggests that the factors contributing to the confusion include different types and doses of oxidants, different cell types, as well as different treatment time used in various studies.…”

Section: Discussionmentioning

confidence: 88%

“…For example, apoptosis signal-regulating kinase 1 (ASK1) is normally bound and repressed by Trx in its reduced form. Upon oxidation, two cysteines in the active site of Trx are oxidized, which leads to dissociation of Trx from ASK1 and subsequent activation of ASK1 (29). A recent paper suggests that the mechanism for oxidation-induced ASK1 activation may be more complicated than we originally thought, because a cysteine outside the kinase domain of ASK1 (i.e., Cys 250 ) could also be directly modified by oxidation, which affects its ability to activate JNK and to mediate H 2 O 2 -induced apoptosis (30).…”

Section: Discussionmentioning

confidence: 99%

Oxidation-induced intramolecular disulfide bond inactivates mitogen-activated protein kinase kinase 6 by inhibiting ATP binding

Diao

Liu

Wong

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Mitogen-activated protein kinase kinase 6 (MKK6) is a member of the mitogen-activated protein kinase (MAPK) kinase (MAP2K) subfamily that specifically phosphorylates and activates the p38 MAPKs. Based on both biochemical and cellular assays, we found that MKK6 was extremely sensitive to oxidation: It was inactivated by oxidation and its kinase activity was fully restored upon treatment with a reducing agent. Detailed mechanistic studies showed that cysteines 109 and 196, two of the six cysteines in MKK6, formed an intramolecular disulfide bond upon oxidation that inactivated MKK6 by inhibiting its ATP binding. This mechanism is distinct from that seen in other redox-sensitive kinases. The two cysteines involved in intramolecular disulfide formation are conserved in all seven members of the MAP2K family. Consistently, we confirmed that other MAP2Ks were also sensitive to oxidation. Our work reveals that MKK6 and other MAP2Ks are a distinct class of cellular redox sensors.

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Redox control of cell fate by MAP kinase: physiological roles of ASK1-MAP kinase pathway in stress signaling

Cited by 443 publications

References 92 publications

Hematopoietic Stem Cell Injury Induced by Ionizing Radiation

Hematopoietic Stem Cell Injury Induced by Ionizing Radiation

Roles of Oxidative Stress in the Development and Progression of Breast Cancer

Oxidation-induced intramolecular disulfide bond inactivates mitogen-activated protein kinase kinase 6 by inhibiting ATP binding

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