| pubmed-article:15647742 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15647742 | lifeskim:mentions | umls-concept:C0376466 | lld:lifeskim |
| pubmed-article:15647742 | lifeskim:mentions | umls-concept:C1171362 | lld:lifeskim |
| pubmed-article:15647742 | lifeskim:mentions | umls-concept:C0597712 | lld:lifeskim |
| pubmed-article:15647742 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15647742 | pubmed:dateCreated | 2005-1-28 | lld:pubmed |
| pubmed-article:15647742 | pubmed:abstractText | Bcl-2 plays a pivotal role in the control of cell death and is upregulated by ischemic tolerance. Because Bcl-2 expression is regulated by the transcription factor cyclic AMP response element-binding protein (CREB), we investigated the role of CREB activation in two models of ischemic preconditioning: focal ischemic tolerance after middle cerebral artery occlusion (MCAO) and in vitro ischemic tolerance modeled by oxygen-glucose deprivation (OGD). After preconditioning ischemia (30 minutes MCAO or 30 minutes OGD), phosphorylation of CREB was increased, and there was an increased interaction between the bcl-2 cyclic AMP-responsive element (CRE) promoter and nuclear proteins after preconditioning ischemia in vivo and in vitro. Chromatin immunoprecipitation revealed an increased interaction between CREB-binding protein and the bcl-2 CRE rather than CREB, after preconditioning ischemia. Ischemic tolerance was blocked by a CRE decoy oligonucleotide, which also blocked Bcl-2 expression. The protein kinase A inhibitor H89, the calcium/calmodulin kinase inhibitor KN62, and the MEK inhibitor U0126 blocked ischemic tolerance, but not the phosphatidylinositol 3-kinase inhibitor LY294002. H89, KN62, and U0126 reduced CREB activation and Bcl-2 expression. Taken together, these data suggest that after ischemic preconditioning CREB activation regulates the expression of the prosurvival protein Bcl-2. | lld:pubmed |
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| pubmed-article:15647742 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15647742 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15647742 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15647742 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15647742 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:15647742 | pubmed:issn | 0271-678X | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:VanS LSL | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:ImpeySorenS | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:SimonRoger... | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:MinamiManabuM | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:MellerRobertR | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:HenshallDavid... | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:LanJing-QuanJ... | lld:pubmed |
| pubmed-article:15647742 | pubmed:author | pubmed-author:CameronJennif... | lld:pubmed |
| pubmed-article:15647742 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15647742 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:15647742 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15647742 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15647742 | pubmed:pagination | 234-46 | lld:pubmed |
| pubmed-article:15647742 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15647742 | pubmed:meshHeading | pubmed-meshheading:15647742... | lld:pubmed |
| pubmed-article:15647742 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15647742 | pubmed:articleTitle | CREB-mediated Bcl-2 protein expression after ischemic preconditioning. | lld:pubmed |
| pubmed-article:15647742 | pubmed:affiliation | RS Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA. rmeller@downeurobiology.org | lld:pubmed |
| pubmed-article:15647742 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15647742 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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