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• W4247353955 abstract "IUBMB LifeVolume 71, Issue 1 p. 8-8 Issue HighlightsFree Access Issue Highlights First published: 19 December 2018 https://doi.org/10.1002/iub.1998AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat 57 Ubiquitin-Independent, Proteasome-Mediated Targeted Degradation of KRAS in Pancreatic Adenocarcinoma Cells Using an Engineered Ornithine Decarboxylase/Antizyme System Yihui Ma, Jingjing Xu, Pei Huang, Xue Bai, Hanqing Gao The ornithine decarboxylase/antizyme (ODC/AZ) system is another protein degradation pathway that exists in nature. The formation of ODC and protein substrate complex through direct combination can promote its degradation by the 26S proteasome without ubiquitination, which can be catalyzed by AZ. We designed and reconstructed a chimeric fusion protein (named RC-ODC), and confirmed it can interact with the mutant KRAS oncoprotein in a co-immunoprecipitation assay. The introduction of both RC-ODC and AZ resulted in degradation of the exogenous and endogenous mutant KRAS oncoprotein at the post-translational level independent of ubiquitiantion in vitro. Along with a decreased KRAS level, suppression of PANC-1 cell proliferation was detected in vitro and in vivo. 66 Role of Reciprocal Interaction Between Autophagy and Endoplasmic Reticulum Stress in Apoptosis of Human Bronchial Epithelial Cells Induced by Cigarette Smoke Extract Baimei He, Qiong Chen, Dongbo Zhou, Lijing Wang, Zhaoqian Liu Treatment with cigarette smoke extract (CSE) induced apoptosis, autophagy, and expression of endoplasmic reticulum stress (ERS)-related proteins in human bronchial epithelial (HBE) cells. Furthermore, both NaHS and melatonin enhanced the CSE-induced autophagy, increased GRP78, p-PERK, and p-eIF2α, and decreased CHOP, ATF4, and caspase-4. Results also indicate both NaHS and melatonin activate SIRT1/ORP150 pathway, and then regulates the reciprocal interaction between autophagy and ERS, thereby attenuating the CSE-induced apoptosis in HBE cells. 125 MicroRNA-146a Sponge Therapy Suppresses Neointimal Formation in Rat Vein Grafts Bo-Jun Cao, Xiao-Wen Wang, Lei Zhu, Rong-Jiang Zou, Zhi-Qian Lu MicroRNA-146a (miR-146a) levels are substantially elevated in rat vein grafts at 7, 14, and 28 days post-grafting. miR-146a sponge gene transduction effectively reduces the expression of miR-146a both in cultured vascular smooth muscle cells (VSMCs) and vein grafts. Knocking-down miR-146a expression markedly attenuates VSMC proliferation and migration. Consistent with this, miR-146a sponge gene therapy significantly attenuates neointimal formation and also improves blood flow in the vein grafts, suggesting its potential therapeutic application for prevention of vein graft failure. REFERENCES 1Ma, Y., Xu, J., Huang, P., Bai, X., and Gao, H. Ubiquitin-independent, Proteasome-mediated Targeted Degradation of KRAS in Pancreatic Adenocarcinoma Cells Using an Engineered Ornithine Decarboxylase/Antizyme System. IUBMB Life. 2019, 71, 57– 65. Wiley Online LibraryCASGoogle Scholar 2 He, Y., Chen, Q., Zhou, D., Wang, L., and Liu, Z. Role of Reciprocal Interaction Between Autophagy and Endoplasmic Reticulum Stress in Apoptosis of Human Bronchial Epithelial Cells Induced by Cigarette Smoke Extract. IUBMB Life. 2019, 71, 66– 80. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar 3 Cao, B.-J., Wang, X.-W., Zhu, L., Zou, R.-J., Lu, Z.-Q. MicroRNA-146a Sponge Therapy Suppresses Neointimal Formation in Rat Vein Grafts. IUBMB Life. 2019, 71, 125– 133. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Volume71, Issue1January 2019Pages 8-8 ReferencesRelatedInformation" @default.
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