Journal
FRONTIERS IN IMMUNOLOGY
Volume 4, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2013.00514
Keywords
thioredoxin; Txnip; redoxisome; inflammation; diabetes mellitus; redox regulation
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Funding
- Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan
- Program for Promotion of Fundamental Studies in Health Sciences of National Institute of Biomedical Innovation (NIBIO)
- World Class University through Ewha Womans University [R31-10010]
- Uehara memorial research foundation
- Japan Society for the Promotion of Science (JSPS)
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During the past few decades, it has been widely recognized that Reduction-Oxidation (redox) responses occurring at the intra- and extra-cellular levels are one of most important biological phenomena and dysregulated redox responses are involved in the initiation and progression of multiple diseases.Thioredoxin1 (Trx1) andThioredoxin2 (Trx2), mainly located in the cytoplasm and mitochondria, respectively, are ubiquitously expressed in variety of cells and control cellular reactive oxygen species by reducing the disulfides into thiol groups. Thioredoxin interacting protein (Txnip/thioredoxin binding protein-2/vitamin D3 upregulated protein) directly binds to Trx1 and Trx2 (Trx) and inhibit the reducing activity of Trx through their disulfide exchange. Recent studies have revealed that Trx1 and Txnip are involved in some critical redox-dependent signal pathways including NLRP-3 inflammasome activation in a redox-dependent manner. Therefore, Trx/Txnip, a redox-sensitive signaling complex is a regulator of cellular redox status and has emerged as a key component in the link between redox regulation and the pathogenesis of diseases. Here, we review the novel functional concept of the redox-related protein complex, named Redoxisome, consisting of Trx/Txnip, as a critical regulator for intra- and extra-cellular redox signaling, involved in the pathogenesis of various diseases such as cancer, autoimmune disease, and diabetes.
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