Ciliary defects caused by dysregulation of O-GlcNAc modification are associated with diabetic complications.
作者信息
Yu Fan, Guo Song, Li Te, Ran Jie, Zhao Wei, Li Dengwen, Liu Min, Yan Xiumin, Yang Xiaoyong, Zhu Xueliang, Zhou Jun
机构信息
State Key Laboratory of Medicinal Chemical Biology, Colleges of Life Sciences and Pharmacy, Nankai University, 300071, Tianjin, China.
Shandong Provincial Key Laboratory of Animal Resistance Biology, College of Life Sciences, Shandong Normal University, 250014, Jinan, Shandong, China.
出版信息
Cell Res. 2019 Feb;29(2):171-173. doi: 10.1038/s41422-018-0114-7. Epub 2018 Nov 14.
Abstract
摘要
相似文献
1
Ciliary defects caused by dysregulation of O-GlcNAc modification are associated with diabetic complications.
Cell Res. 2019 Feb;29(2):171-173. doi: 10.1038/s41422-018-0114-7. Epub 2018 Nov 14.
2
O-GlcNAc modification, insulin signaling and diabetic complications.
Diabetes Metab. 2010 Dec;36(6 Pt 1):423-35. doi: 10.1016/j.diabet.2010.09.001. Epub 2010 Nov 11.
3
New insights: A role for O-GlcNAcylation in diabetic complications.
Crit Rev Biochem Mol Biol. 2016 May-Jun;51(3):150-61. doi: 10.3109/10409238.2015.1135102. Epub 2016 Jan 24.
4
The mitochondrial O-linked N-acetylglucosamine transferase (mOGT) in the diabetic patient could be the initial trigger to develop Alzheimer disease.
Exp Gerontol. 2014 Oct;58:198-202. doi: 10.1016/j.exger.2014.08.008. Epub 2014 Aug 19.
5
Elevation of the post-translational modification of proteins by O-linked N-acetylglucosamine leads to deterioration of the glucose-stimulated insulin secretion in the pancreas of diabetic Goto-Kakizaki rats.
Glycobiology. 2007 Feb;17(2):127-40. doi: 10.1093/glycob/cwl067. Epub 2006 Nov 9.
6
Yeast cells as an assay system for in vivo O-GlcNAc modification.
Biochim Biophys Acta Gen Subj. 2017 May;1861(5 Pt A):1159-1167. doi: 10.1016/j.bbagen.2017.03.002. Epub 2017 Mar 2.
7
Intracellular glycosylation and development.
Biochim Biophys Acta. 2002 Dec 19;1573(3):336-45. doi: 10.1016/s0304-4165(02)00401-4.
8
T cell development and the physiological role of O-GlcNAc.
FEBS Lett. 2018 Dec;592(23):3943-3949. doi: 10.1002/1873-3468.13159. Epub 2018 Jun 29.
9
Intracellular protein O-GlcNAc modification integrates nutrient status with transcriptional and metabolic regulation.
Adv Cancer Res. 2015;126:137-66. doi: 10.1016/bs.acr.2014.12.003. Epub 2015 Feb 7.
10
Tools for probing and perturbing O-GlcNAc in cells and in vivo.
Curr Opin Chem Biol. 2013 Oct;17(5):719-28. doi: 10.1016/j.cbpa.2013.06.030. Epub 2013 Jul 30.
引用本文的文献
1
Post-Translational Modifications in Cilia and Ciliopathies.
Adv Sci (Weinh). 2025 Aug;12(31):e16562. doi: 10.1002/advs.202416562. Epub 2025 May 28.
2
UFMylation Modulates OFIP Stability and Centrosomal Localization.
J Clin Lab Anal. 2025 Mar;39(6):e70004. doi: 10.1002/jcla.70004. Epub 2025 Mar 10.
3
Resveratrol and quercetin protect from Benzo(a)pyrene-induced autophagy in retinal pigment epithelial cells.
Int Ophthalmol. 2024 Feb 6;44(1):12. doi: 10.1007/s10792-024-02957-6.
4
Pathologically relevant aldoses and environmental aldehydes cause cilium disassembly via formyl group-mediated mechanisms.
J Mol Cell Biol. 2024 Jul 1;16(1). doi: 10.1093/jmcb/mjad079.
5
O-GlcNAcylation Regulates Centrosome Behavior and Cell Polarity to Reduce Pulmonary Fibrosis and Maintain the Epithelial Phenotype.
Adv Sci (Weinh). 2023 Dec;10(36):e2303545. doi: 10.1002/advs.202303545. Epub 2023 Nov 14.
6
Regulation of Primary Cilium Length by O-GlcNAc during Neuronal Development in a Human Neuron Model.
Cells. 2023 May 31;12(11):1520. doi: 10.3390/cells12111520.
7
Functions and Diseases of the Retinal Pigment Epithelium.
Front Pharmacol. 2021 Jul 28;12:727870. doi: 10.3389/fphar.2021.727870. eCollection 2021.
8
Intraflagellar Transport Proteins as Regulators of Primary Cilia Length.
Front Cell Dev Biol. 2021 May 19;9:661350. doi: 10.3389/fcell.2021.661350. eCollection 2021.
9
CYLD deficiency causes auditory neuropathy due to reduced neurite outgrowth.
J Clin Lab Anal. 2021 Jun;35(6):e23783. doi: 10.1002/jcla.23783. Epub 2021 May 2.
10
Centrosomes: Til O-GlcNAc Do Us Apart.
Front Endocrinol (Lausanne). 2021 Feb 1;11:621888. doi: 10.3389/fendo.2020.621888. eCollection 2020.
本文引用的文献
1
Glucose deprivation induces primary cilium formation through mTORC1 inactivation.
J Cell Sci. 2018 Jan 8;131(1):jcs208769. doi: 10.1242/jcs.208769.
2
Early ciliary and prominin-1 dysfunctions precede neurogenesis impairment in a mouse model of type 2 diabetes.
Neurobiol Dis. 2017 Dec;108:13-28. doi: 10.1016/j.nbd.2017.07.010. Epub 2017 Jul 23.
3
Diabetes mellitus statistics on prevalence and mortality: facts and fallacies.
Nat Rev Endocrinol. 2016 Oct;12(10):616-22. doi: 10.1038/nrendo.2016.105. Epub 2016 Jul 8.
4
Diabetes-associated dysregulation of O-GlcNAcylation in rat cardiac mitochondria.
Proc Natl Acad Sci U S A. 2015 May 12;112(19):6050-5. doi: 10.1073/pnas.1424017112. Epub 2015 Apr 27.
5
Nutrient regulation of signaling, transcription, and cell physiology by O-GlcNAcylation.
Cell Metab. 2014 Aug 5;20(2):208-13. doi: 10.1016/j.cmet.2014.07.014.
6
Mechanisms of diabetic complications.
Physiol Rev. 2013 Jan;93(1):137-88. doi: 10.1152/physrev.00045.2011.
7
A neutral diphosphate mimic crosslinks the active site of human O-GlcNAc transferase.
Nat Chem Biol. 2011 Nov 13;8(1):72-7. doi: 10.1038/nchembio.711.
8
Molecular understanding of hyperglycemia's adverse effects for diabetic complications.
JAMA. 2002 Nov 27;288(20):2579-88. doi: 10.1001/jama.288.20.2579.
Zotero 插件