BMB Reports 2018; 51(12): 654-659
Tat-ATOX1 inhibits inflammatory responses via regulation of MAPK and NF-κB pathways
Dae Won Kim2,#, Min Jea Shin1,#, Yeon Joo Choi1,#, Hyun Jung Kwon2, Sung Ho Lee3, Sunghou Lee4, Jinseu Park1, Kyu Hyung Han1, Won Sik Eum1,* and Soo Young Choi1,*
1Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, 2Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 25457, 3R&D Center, Lumieye Genetics Co., Ltd., Seoul 06198, 4Department of Green Chemical Engineering, Sangmyung University, Cheonan 31066, Korea
Correspondence to: *Corresponding authors. Soo Young Choi, Tel: +82-33-248-2112; Fax: +82-33-248-3202; E-mail:; Won Sik Eum, Tel: +82-33-248-3221; Fax: +82-33-248-3202; E-mail:
#These authors contributed equally to this work.
Received: October 26, 2018; Revised: November 9, 2018; Accepted: November 21, 2018; Published online: December 31, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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-κB) 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-κB, Protein therapy, Tat-ATOX1

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