دورية أكاديمية
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NR4A1 counteracts JNK activation incurred by ER stress or ROS in pancreatic β-cells for protection.

التفاصيل البيبلوغرافية
العنوان: NR4A1 counteracts JNK activation incurred by ER stress or ROS in pancreatic β-cells for protection.
المؤلفون: Pu ZQ; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Liu D; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Lobo Mouguegue HPP; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Jin CW; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Sadiq E; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Qin DD; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Yu TF; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Zong C; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Chen JC; Blood Transfusion Department, Qilu Hospital of Shandong University, Jinan, China., Zhao RX; Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China., Lin JY; Department of Physiology, Shandong University School of Medicine, Jinan, China., Cheng J; Department of Physiology, Shandong University School of Medicine, Jinan, China., Yu X; Department of Physiology, Shandong University School of Medicine, Jinan, China.; Key Laboratory of Protein Sciences for Chronic Degenerative Diseases in Universities of Shandong (Shandong University), Jinan, China., Li X; Department of Cell Biology, Shandong University School of Medicine, Jinan, China., Zhang YC; Department of Endocrinology, Qingdao Municipal Hospital, Qingdao, China., Liu YT; Department of Endocrinology, Qingdao Municipal Hospital, Qingdao, China., Guan QB; Department of Endocrinology, Shandong Provincial Hospital, Affiliated to Shandong University, Jinan, China., Wang XD; Department of Cell Biology, Shandong University School of Medicine, Jinan, China.; Key Laboratory of Protein Sciences for Chronic Degenerative Diseases in Universities of Shandong (Shandong University), Jinan, China.
المصدر: Journal of cellular and molecular medicine [J Cell Mol Med] 2020 Dec; Vol. 24 (24), pp. 14171-14183. Date of Electronic Publication: 2020 Oct 30.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101083777 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1582-4934 (Electronic) Linking ISSN: 15821838 NLM ISO Abbreviation: J Cell Mol Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford, England : Wiley-Blackwell
Original Publication: Bucharest : "Carol Davila" University Press, 2000-
مواضيع طبية MeSH: Endoplasmic Reticulum Stress*, Insulin-Secreting Cells/*metabolism , JNK Mitogen-Activated Protein Kinases/*metabolism , Nuclear Receptor Subfamily 4, Group A, Member 1/*metabolism , Reactive Oxygen Species/*metabolism, Animals ; Cell Line ; Gene Expression Regulation ; Hydrogen Peroxide/metabolism ; MAP Kinase Kinase 4/metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Nuclear Receptor Subfamily 4, Group A, Member 1/genetics ; Phosphorylation ; Promoter Regions, Genetic ; Protein Binding ; Ubiquitination
مستخلص: Sustained hyperglycaemia and hyperlipidaemia incur endoplasmic reticulum stress (ER stress) and reactive oxygen species (ROS) overproduction in pancreatic β-cells. ER stress or ROS causes c-Jun N-terminal kinase (JNK) activation, and the activated JNK triggers apoptosis in different cells. Nuclear receptor subfamily 4 group A member 1 (NR4A1) is an inducible multi-stress response factor. The aim of this study was to explore the role of NR4A1 in counteracting JNK activation induced by ER stress or ROS and the related mechanism. qPCR, Western blotting, dual-luciferase reporter and ChIP assays were applied to detect gene expression or regulation by NR4A1. Immunofluorescence was used to detect a specific protein expression in β-cells. Our data showed that NR4A1 reduced the phosphorylated JNK (p-JNK) in MIN6 cells encountering ER stress or ROS and reduced MKK4 protein in a proteasome-dependent manner. We found that NR4A1 increased the expression of cbl-b (an E3 ligase); knocking down cbl-b expression increased MKK4 and p-JNK levels under ER stress or ROS conditions. We elucidated that NR4A1 enhanced the transactivation of cbl-b promoter by physical association. We further confirmed that cbl-b expression in β-cells was reduced in NR4A1-knockout mice compared with WT mice. NR4A1 down-regulates JNK activation by ER stress or ROS in β-cells via enhancing cbl-b expression.
(© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)
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فهرسة مساهمة: Keywords: ER stress; NR4A1 (Nur77); ROS; cbl-b; p-JNK; pancreatic β-cells
المشرفين على المادة: 0 (Nr4a1 protein, mouse)
0 (Nuclear Receptor Subfamily 4, Group A, Member 1)
0 (Reactive Oxygen Species)
BBX060AN9V (Hydrogen Peroxide)
EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
EC 2.7.12.2 (MAP Kinase Kinase 4)
تواريخ الأحداث: Date Created: 20201030 Date Completed: 20210519 Latest Revision: 20221005
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC7754045
DOI: 10.1111/jcmm.16028
PMID: 33124187
قاعدة البيانات: MEDLINE
الوصف
تدمد:1582-4934
DOI:10.1111/jcmm.16028