| pubmed-article:11487632 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C0174680 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C0246957 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C2754100 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:11487632 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:11487632 | pubmed:issue | 16 | lld:pubmed |
| pubmed-article:11487632 | pubmed:dateCreated | 2001-8-6 | lld:pubmed |
| pubmed-article:11487632 | pubmed:abstractText | Systemic administration of the glutamic acid analog kainic acid (KA) causes neuronal cell death in brain-vulnerable regions, such as the piriform cortex, hippocampus, and amygdala in rats. We investigated the relationship between the KA-induced neuronal apoptosis and expression of cyclin-dependent kinase 4 (CDK4) and cyclin D1, key regulators of cell cycle progression. Expression of CDK4 and cyclin D1 was upregulated in neurons of the rat piriform cortex and amygdala 1-3 d after KA administration in vivo. CDK4 and cyclin D1 proteins were induced in the cytoplasm and nuclei of neurons, with a concomitant increase of CDK4- and cyclin D1-positive microglia in the affected areas. Continuous infusion of 100 microm CDK4 or cyclin D1 antisense oligonucleotides into the lateral ventricle using mini-osmotic pumps suppressed the excitotoxin-induced neuronal cell death in the piriform cortex and basolateral amygdaloid nucleus, whereas sense oligonucleotides exhibited no such effect. Although KA administration causes prolonged c-Fos expression in the vulnerable regions that preceded the induction of neuronal apoptosis, the CDK4 or cyclin D1 antisense oligonucleotides exhibited no suppressive effect on c-Fos levels. Our results suggest that CDK4 and cyclin D1 are essential for KA-induced neuronal apoptosis in vivo. | lld:pubmed |
| pubmed-article:11487632 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11487632 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11487632 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11487632 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11487632 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11487632 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11487632 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:11487632 | pubmed:issn | 1529-2401 | lld:pubmed |
| pubmed-article:11487632 | pubmed:author | pubmed-author:ChibaTT | lld:pubmed |
| pubmed-article:11487632 | pubmed:author | pubmed-author:InoHH | lld:pubmed |
| pubmed-article:11487632 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11487632 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11487632 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:11487632 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11487632 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11487632 | pubmed:pagination | 6086-94 | lld:pubmed |
| pubmed-article:11487632 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11487632 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11487632 | pubmed:articleTitle | Cyclin-dependent kinase 4 and cyclin D1 are required for excitotoxin-induced neuronal cell death in vivo. | lld:pubmed |
| pubmed-article:11487632 | pubmed:affiliation | Department of Neurobiology (C1), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. ino@med.m.chiba-u.ac.jp | lld:pubmed |
| pubmed-article:11487632 | pubmed:publicationType | Journal Article | lld:pubmed |
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