한빛사 논문
Jinhong Park PhDa,b,∗, Hyun Jae Lee PhDc,∗, Doona Song PhDd,∗, Mia Gi PhDc,∗, Sungwoo Jo BSa, Dong-kyu Jeon BSa, Yohan Seo PhDa, Bomin Kim BSe,f, Ho Lee PhDg, Wan Namkung PhDa,b,‡, Gyoonhee Han PhDa,b,d,‡, Jae Young Choi MD, PhDc,‡
a College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Incheon, Korea
b Department of Integrated OMICS for Biomedical Science, Yonsei University, Seoul, Korea
c Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea
d Translational Research Center for Protein Function Control, Department of Biotechnology, Yonsei University, Seoul, Korea
e Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea
f Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea
g Graduate School of Cancer Science and Policy, National Cancer Center, Goyang-si, Korea
* These authors contributed equally to this work.
‡ These authors contributed equally to this work as co-senior authors.
Abstract
The transmembrane anion exchanger pendrin (SCL26A4) exchanges Cl− with bases, such as HCO3−, I−, and SCN−, and is the most highly upregulated gene in endobronchial biopsies from patients with asthma.1, 2 Interestingly, patients with mutant pendrin have a low prevalence of asthma, and pendrin-null mice show reduced allergic airway inflammation.3, 4, 5 These observations indicate that pendrin is a novel target for allergic asthma. In this study, we identified a novel pendrin inhibitor, YS-01 (2-(4-(tert-butyl)phenyl)-4-(thiophen-2-ylmethylene)oxazol-5(4H)-one), with strong therapeutic effects on allergic inflammation in a mouse model of ovalbumin (OVA)-induced asthma.
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