| Inhibition of cerebral ischemia/reperfusion-induced injury by adenovirus expressed C-terminal amino acids of GluR6. | |
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MedLine Citation:
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PMID: 19747468 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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GluR6 kainate receptor subunit is largely expressed in hippocampus of brain regions and plays an important role in brain ischemia/reperfusion-mediated neuronal cell death. Our previous researches have shown that cerebral ischemia/reperfusion could facilitate the assembly of GluR6 and postsynaptic density protein 95(PSD95) as well as mixed lineage kinase 3(MLK3) and further induce the activation of c-Jun NH2-terminal kinase 3(JNK3), leading to neuronal death of hippocampal CA1. Here, we show that over-expression of C-terminal amino acids of GluR6 can interrupt the combination of GluR6 with PSD95, inhibit the assembly of GluR6.PSD-95.MLK3 signaling module, suppress the activation of JNK3 and the downstream signaling pathway. Thus, our results imply that over-expression of C-terminal amino acids of GluR6 induce neuroprotection against ischaemic brain injury in rat hippocampal CA1 region via suppressing proapoptosis signaling pathways, which can be an experimental foundation for gene therapy of stroke. |
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Authors:
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Ting Li; Hong-Min Yu; Ya-Feng Sun; Yuan-Jian Song; Guang-Yi Zhang; Dong-Sheng Pei |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-09-09 |
Journal Detail:
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Title: Brain research Volume: 1300 ISSN: 1872-6240 ISO Abbreviation: Brain Res. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-10-27 Completed Date: 2010-01-05 Revised Date: 2010-01-13 |
Medline Journal Info:
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Nlm Unique ID: 0045503 Medline TA: Brain Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 169-76 Citation Subset: IM |
Affiliation:
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Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenoviridae
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metabolism Analysis of Variance Animals Blotting, Western Brain Ischemia / metabolism, pathology, therapy* CA1 Region, Hippocampal / metabolism, pathology Cell Death / physiology Cell Fractionation Cell Survival / genetics Cytoprotection Gene Transfer Techniques Genetic Vectors Intracellular Signaling Peptides and Proteins / metabolism MAP Kinase Kinase Kinases / metabolism Male Membrane Proteins / metabolism Mitogen-Activated Protein Kinase 10 / metabolism Neurons / metabolism Phosphorylation Rats Rats, Sprague-Dawley Receptors, Kainic Acid / metabolism* Reperfusion Injury / metabolism, pathology, therapy* Signal Transduction / physiology Staining and Labeling Subcellular Fractions / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Dlgh4 protein, rat; 0/Gluk2 kainate receptor; 0/Intracellular Signaling Peptides and Proteins; 0/Membrane Proteins; 0/Receptors, Kainic Acid; EC 2.7.1.-/Mitogen-Activated Protein Kinase 10; EC 2.7.11.25/MAP Kinase Kinase Kinases; EC 2.7.11.25/mitogen-activated protein kinase kinase kinase 11 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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