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http://dx.doi.org/10.5483/BMBRep.2018.51.12.248

Tat-ATOX1 inhibits inflammatory responses via regulation of MAPK and NF-κB pathways  

Kim, Dae Won (Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University)
Shin, Min Jea (Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University)
Choi, Yeon Joo (Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University)
Kwon, Hyun Jung (Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University)
Lee, Sung Ho (R&D Center, Lumieye Genetics Co., Ltd.)
Lee, Sunghou (Department of Green Chemical Engineering, Sangmyung University)
Park, Jinseu (Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University)
Han, Kyu Hyung (Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University)
Eum, Won Sik (Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University)
Choi, Soo Young (Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University)
Publication Information
BMB Reports / v.51, no.12, 2018 , pp. 654-659 More about this Journal
Abstract
Antioxidant 1 (ATOX1) protein has been reported to exhibit various protective functions, including antioxidant and chaperone. However, the effects of ATOX1 on the inflammatory response has not been fully elucidated. Thus, we prepared cell permeable Tat-ATOX1 and studied the effects on lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. Experimental results showed that transduced Tat-ATOX1 protein significantly suppressed LPS-induced intracellular reactive oxygen species (ROS). Also, Tat-ATOX1 protein markedly inhibited LPS- and TPA-induced inflammatory responses by decreasing cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) and further inhibited phosphorylation of mitogen activated protein kinases (MAPKs; JNK, ERK and p38) and the nuclear factor-kappaB ($NF-{\kappa}B$) signaling pathway. These results indicate that the Tat-ATOX1 protein has a pivotal role in inflammation via inhibition of inflammatory responses, suggesting Tat-ATOX1 protein may offer a therapeutic strategy for inflammation.
Keywords
Inflammation; MAPK; $NF-{\kappa}B$; Protein therapy; Tat-ATOX1;
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