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Int. J. Mol. Sci. 2016, 17(12), 2059; doi:10.3390/ijms17122059

Roles of Erythroid Differentiation Regulator 1 (Erdr1) on Inflammatory Skin Diseases

1,†
,
2,†
,
3,†,* and 1,2,†,*
1
Department of Biological Sciences, Sookmyung Women’s University, Seoul 04310, Korea
2
Department of Cosmetic Sciences, Sookmyung Women’s University, Seoul 04310, Korea
3
Department of Dermatology, Yeouido St. Mary’s Hospital, The Catholic University of Korea, Seoul 07345, Korea
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Chris Jackson
Received: 21 October 2016 / Revised: 30 November 2016 / Accepted: 5 December 2016 / Published: 8 December 2016
(This article belongs to the Special Issue Inflammatory Skin Conditions)
View Full-Text   |   Download PDF [977 KB, uploaded 8 December 2016]   |  

Abstract

Erythroid Differentiation Regulator 1 (Erdr1) is known as a hemoglobin synthesis factor which also regulates cell survival under conditions of stress. In addition, previous studies have revealed the effects of Erdr1 on cancer progression and its negative correlation with interleukin (IL)-18, a pro-inflammatory cytokine. Based on this evidence, the therapeutic effects of Erdr1 have been demonstrated in several inflammatory skin diseases such as malignant skin cancer, psoriasis, and rosacea. This article reviews the roles of Erdr1 in skin inflammation, suggesting that Erdr1 is a potential therapeutic molecule on inflammatory disorders. View Full-Text
Keywords: Erdr1; IL-18; cutaneous inflammation; melanoma; psoriasis; rosacea Erdr1; IL-18; cutaneous inflammation; melanoma; psoriasis; rosacea
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Houh, Y.K.; Kim, K.E.; Park, H.J.; Cho, D. Roles of Erythroid Differentiation Regulator 1 (Erdr1) on Inflammatory Skin Diseases. Int. J. Mol. Sci. 2016, 17, 2059.

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