转谷氨酰胺酶与神经退行性变
Transglutaminases and neurodegeneration.
作者信息
Jeitner Thomas M, Pinto John T, Krasnikov Boris F, Horswill Mark, Cooper Arthur J L
机构信息
Red Anvil, LLC, Milwaukee, Wisconsin, USA.
出版信息
J Neurochem. 2009 May;109 Suppl 1(Suppl 1):160-6. doi: 10.1111/j.1471-4159.2009.05843.x.
Abstract
Transglutaminases (TGs) are Ca2+-dependent enzymes that catalyze a variety of modifications of glutaminyl (Q) residues. In the brain, these modifications include the covalent attachment of a number of amine-bearing compounds, including lysyl (K) residues and polyamines, which serve to either regulate enzyme activity or attach the TG substrates to biological matrices. Aberrant TG activity is thought to contribute to Alzheimer disease, Parkinson disease, Huntington disease, and supranuclear palsy. Strategies designed to interfere with TG activity have some benefit in animal models of Huntington and Parkinson diseases. The following review summarizes the involvement of TGs in neurodegenerative diseases and discusses the possible use of selective inhibitors as therapeutic agents in these diseases.
摘要
转谷氨酰胺酶（TGs）是一类依赖钙离子的酶，可催化谷氨酰胺（Q）残基的多种修饰。在大脑中，这些修饰包括许多含胺化合物的共价连接，其中包括赖氨酸（K）残基和多胺，它们要么用于调节酶活性，要么将TG底物附着于生物基质。TG活性异常被认为与阿尔茨海默病、帕金森病、亨廷顿病和核上性麻痹有关。旨在干扰TG活性的策略在亨廷顿病和帕金森病的动物模型中具有一定益处。以下综述总结了TGs在神经退行性疾病中的作用，并讨论了选择性抑制剂作为这些疾病治疗药物的潜在用途。
相似文献
1
Transglutaminases and neurodegeneration.
J Neurochem. 2009 May;109 Suppl 1(Suppl 1):160-6. doi: 10.1111/j.1471-4159.2009.05843.x.
2
Transglutaminases as possible therapeutic targets in neurodegenerative diseases.
Recent Pat CNS Drug Discov. 2010 Nov;5(3):195-202. doi: 10.2174/157488910793362430.
3
Transglutaminase activity as a possible therapeutical target in neurodegenerative diseases.
Recent Pat CNS Drug Discov. 2013 Dec;8(3):235-42. doi: 10.2174/1574889808666131128105630.
4
Transglutaminases - possible drug targets in human diseases.
Curr Drug Targets CNS Neurol Disord. 2004 Apr;3(2):99-104. doi: 10.2174/1568007043482552.
5
Transglutaminase inhibition as a possible therapeutical approach to protect cells from death in neurodegenerative diseases.
Recent Pat CNS Drug Discov. 2013 Aug;8(2):161-8. doi: 10.2174/15748898113089990001.
6
Possible physiopathological effects of the transglutaminase activity on the molecular mechanisms responsible for human neurodegenerative diseases.
Recent Pat CNS Drug Discov. 2014;9(2):76-84. doi: 10.2174/1574889809666141111160124.
7
Possible physiopathological roles of the transglutaminase activity in the etiopathogenesis of human neurodegenerative diseases.
Recent Pat CNS Drug Discov. 2014;9(2):101-9. doi: 10.2174/1574889809666140613114850.
8
Role of the transglutaminase enzymes in the nervous system and their possible involvement in neurodegenerative diseases.
Curr Med Chem. 2009;16(36):4767-73. doi: 10.2174/092986709789909594.
9
Transglutaminase-catalyzed post-translational modifications of proteins in the nervous system and their possible involvement in neurodegenerative diseases.
CNS Neurol Disord Drug Targets. 2008 Oct;7(4):370-5. doi: 10.2174/187152708786441821.
10
In situ enzymatic activity of transglutaminase isoforms on brain tissue sections of rodents: A new approach to monitor differences in post-translational protein modifications during neurodegeneration.
Brain Res. 2016 Jan 15;1631:22-33. doi: 10.1016/j.brainres.2015.11.027. Epub 2015 Nov 23.
引用本文的文献
1
Development of peptide-based biosensors for detecting cross-linking and deamidation activities of transglutaminases.
Amino Acids. 2023 Jun;55(6):807-819. doi: 10.1007/s00726-023-03272-7. Epub 2023 May 10.
2
The Outside-In Journey of Tissue Transglutaminase in Cancer.
Cells. 2022 May 29;11(11):1779. doi: 10.3390/cells11111779.
3
The Rate of Decrease in Brain Perfusion in Progressive Supranuclear Palsy and Corticobasal Syndrome May Be Impacted by Glycemic Variability-A Pilot Study.
Front Neurol. 2021 Nov 8;12:767480. doi: 10.3389/fneur.2021.767480. eCollection 2021.
4
Transglutaminase 6 Is Colocalized and Interacts with Mutant Huntingtin in Huntington Disease Rodent Animal Models.
Int J Mol Sci. 2021 Aug 18;22(16):8914. doi: 10.3390/ijms22168914.
5
Role of Transglutaminase 2 in Cell Death, Survival, and Fibrosis.
Cells. 2021 Jul 20;10(7):1842. doi: 10.3390/cells10071842.
6
Probing tissue transglutaminase mediated vascular smooth muscle cell aging using a novel transamidation-deficient Tgm2-C277S mouse model.
Cell Death Discov. 2021 Jul 29;7(1):197. doi: 10.1038/s41420-021-00543-8.
7
Neither a Novel Tau Proteinopathy nor an Expansion of a Phenotype: Reappraising Clinicopathology-Based Nosology.
Int J Mol Sci. 2021 Jul 7;22(14):7292. doi: 10.3390/ijms22147292.
8
Zinc as a modulator of transglutaminase activity - Laboratory and pathophysiological aspects.
J Transl Autoimmun. 2021 Jun 17;4:100110. doi: 10.1016/j.jtauto.2021.100110. eCollection 2021.
9
Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.
J Neuroinflammation. 2020 Oct 14;17(1):301. doi: 10.1186/s12974-020-01955-6.
10
The Tubulin Code in Microtubule Dynamics and Information Encoding.
Dev Cell. 2020 Jul 6;54(1):7-20. doi: 10.1016/j.devcel.2020.06.008.
本文引用的文献
1
Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.
Ann Neurol. 2008 Sep;64(3):332-43. doi: 10.1002/ana.21450.
2
Reversible and competitive cinnamoyl triazole inhibitors of tissue transglutaminase.
Chem Biol Drug Des. 2008 Sep;72(3):189-96. doi: 10.1111/j.1747-0285.2008.00696.x. Epub 2008 Aug 19.
3
Cinnamoyl inhibitors of tissue transglutaminase.
J Org Chem. 2008 Aug 1;73(15):5766-75. doi: 10.1021/jo8004843. Epub 2008 Jun 27.
4
Increased levels of gamma-glutamylamines in Huntington disease CSF.
J Neurochem. 2008 Jul;106(1):37-44. doi: 10.1111/j.1471-4159.2008.05350.x. Epub 2008 Jul 1.
5
Transglutaminase induces protofibril-like amyloid beta-protein assemblies that are protease-resistant and inhibit long-term potentiation.
J Biol Chem. 2008 Jun 13;283(24):16790-800. doi: 10.1074/jbc.M802215200. Epub 2008 Apr 8.
6
Impaired ubiquitin-proteasome system activity in the synapses of Huntington's disease mice.
J Cell Biol. 2008 Mar 24;180(6):1177-89. doi: 10.1083/jcb.200709080.
7
Therapeutic attenuation of mitochondrial dysfunction and oxidative stress in neurotoxin models of Parkinson's disease.
Biochim Biophys Acta. 2008 Mar;1782(3):151-62. doi: 10.1016/j.bbadis.2007.12.006. Epub 2008 Jan 16.
8
Global changes to the ubiquitin system in Huntington's disease.
Nature. 2007 Aug 9;448(7154):704-8. doi: 10.1038/nature06022.
9
Hyaluronic acid induces transglutaminase II to enhance cell motility; role of Rac1 and FAK in the induction of transglutaminase II.
Biotechnol Lett. 2008 Jan;30(1):31-9. doi: 10.1007/s10529-007-9496-1. Epub 2007 Aug 7.
10
Calcium and neurodegeneration.
Aging Cell. 2007 Jun;6(3):337-50. doi: 10.1111/j.1474-9726.2007.00275.x. Epub 2007 Feb 28.
Zotero 插件