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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0018790,
umls-concept:C0019564,
umls-concept:C0022116,
umls-concept:C0030012,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0140145,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0521447,
umls-concept:C1332102,
umls-concept:C1521761,
umls-concept:C2348867,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
1998-5-4
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pubmed:abstractText |
The Ref-1 protein is a bifunctional nuclear enzyme involved in repair of DNA lesions and in redox regulation of DNA-binding activity of AP-1 family members, such as Fos and Jun transcription factors. In the present study, we demonstrate by in situ hybridization that transient global ischemia induced by cardiac arrest activates ref-1 mRNA expression in the granular cells of the rat dentate gyrus after 6 h and in CA1 pyramidal neurons of the hippocampus proper after 24 h, respectively. Immunohistochemical analysis revealed nuclear accumulation of Ref-1 protein in granular cells of the ischemia-resistant dentate gyrus, whereas Ref-1 protein expression progressively decreased in vulnerable CA1 neurons of the post-ischemic hippocampus from 24 h onwards. At the same time point, intense nuclear c-Jun immunoreactivity was observed in both neuronal cell populations. Our data suggest that oxidative stress induced by ischemia-reperfusion may increase neuronal ref-1 expression. However, inability of ref-1 mRNA translation and nuclear translocation of encoded protein in CA1 pyramidal neurons may inhibit repair of oxidative DNA damage or cellular adaptive responses leading to delayed neuronal cell death.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0169-328X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
194-200
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pubmed:dateRevised |
2011-8-4
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pubmed:meshHeading |
pubmed-meshheading:9495540-Animals,
pubmed-meshheading:9495540-Brain,
pubmed-meshheading:9495540-Carbon-Oxygen Lyases,
pubmed-meshheading:9495540-Cell Nucleus,
pubmed-meshheading:9495540-DNA Fragmentation,
pubmed-meshheading:9495540-DNA Repair,
pubmed-meshheading:9495540-DNA-(Apurinic or Apyrimidinic Site) Lyase,
pubmed-meshheading:9495540-Glial Fibrillary Acidic Protein,
pubmed-meshheading:9495540-Heart Arrest,
pubmed-meshheading:9495540-Hippocampus,
pubmed-meshheading:9495540-Immunohistochemistry,
pubmed-meshheading:9495540-In Situ Hybridization,
pubmed-meshheading:9495540-Ischemic Attack, Transient,
pubmed-meshheading:9495540-Male,
pubmed-meshheading:9495540-Neurons,
pubmed-meshheading:9495540-Nuclear Proteins,
pubmed-meshheading:9495540-RNA, Messenger,
pubmed-meshheading:9495540-Rats,
pubmed-meshheading:9495540-Rats, Sprague-Dawley,
pubmed-meshheading:9495540-Reference Values,
pubmed-meshheading:9495540-Transcription, Genetic
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pubmed:year |
1997
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pubmed:articleTitle |
Expression of nuclear redox factor ref-1 in the rat hippocampus following global ischemia induced by cardiac arrest.
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pubmed:affiliation |
Max-Planck-Institut für Neurologische Forschung, Köln, Germany. gillardon@mpin-koeln.mpg.de
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pubmed:publicationType |
Journal Article
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