Bombesin Receptor-Activated Protein (BRAP) Modulates NF-[kappa]B Activation in Bronchial Epithelial Cells by Enhancing HDAC Activity

• Published in: Journal of cellular biochemistry Vol. 117; no. 5; p. 1069
• Main Authors: Liu, Ying, Qin, Xiao-Qun, Weber, Horst Christian, Xiang, Yang, Liu, Chi, Liu, Hui-Jun, Yang, Huan, Jiang, Jianxin, Qu, Xiangping
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc 01.05.2016
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.25406

Our previous studies provided evidence that bombesin receptor-activated protein (BRAP), encoded by C6ORF89, is widely expressed in human airway epithelial cells and may play a role in the stress response of lung epithelia. In this study, we demonstrated that BRAP has a regulatory effect on NF-[kappa]B transcriptional activity in cultured human bronchial epithelial cells (HBECs). BRAP overexpression by gene transfer inhibited both basal and inducible NF-[kappa]B transcriptional activity in HBECs, whereas BRAP knockdown had the opposite effect. BRAP was shown to regulate NF-[kappa]B activity by enhancing histone deacetylase (HDAC) activity. In addition, BRAP might increase HDAC activity that leads to NF-[kappa]B activation via its putative C-terminal domain. Our study suggests that the BRAP protein is an important regulator of immune and inflammatory responses in the human airway epithelium. J. Cell. Biochem. 117: 1069-1077, 2016. © 2015 Wiley Periodicals, Inc.