| pubmed-article:11391701 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0007776 | lld:lifeskim |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0022655 | lld:lifeskim |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0001613 | lld:lifeskim |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0014939 | lld:lifeskim |
| pubmed-article:11391701 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:11391701 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11391701 | pubmed:dateCreated | 2001-6-6 | lld:pubmed |
| pubmed-article:11391701 | pubmed:abstractText | Estrogen replacement therapy in menopausal women has been suggested to be beneficial in preventing the progression of cognitive impairment in Alzheimer disease. We demonstrated previously that the phosphatidylinositol 3-kinase (PI3-K)/Akt signal transduction pathway plays a pivotal role on the neuroprotection provided by 17beta-estradiol against acute glutamate toxicity. In the present study, we investigated the mechanism of neuroprotection against apoptosis because acute glutamate toxicity predominantly induced necrosis. 17beta-estradiol provided neuroprotection against apoptosis induced by staurosporine. This neuroprotection was inhibited by pretreatment with a PI3-K inhibitor, LY294002. An estrogen receptor specific antagonist, ICI182780, also suppressed the neuroprotection provided by 17beta-estradiol. Western blotting analysis demonstrated that treatment with 17beta-estradiol induced the phosphorylation of Akt within 5 min, which was suppressed by pretreatment with LY294002 and ICI182780. Furthermore, 17beta-estradiol induced phosphorylation of the cAMP response element binding protein (CREB) at Ser(133) within 15 min and then upregulated Bcl-2 in a PI3-K/Akt-dependent manner. Because CREB is known to be a transcription factor for Bcl-2, these results suggest that 17beta-estradiol exerts its antiapoptotic effects by CREB phosphorylation and Bcl-2 upregulation via nongenomic activation of the PI3-K/Akt pathway in cultured cortical neurons. | lld:pubmed |
| pubmed-article:11391701 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11391701 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11391701 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11391701 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11391701 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11391701 | pubmed:issn | 0360-4012 | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:HondaKK | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:SawadaHH | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:ShibasakiHH | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:AkaikeAA | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:KiharaTT | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:ShimohamaSS | lld:pubmed |
| pubmed-article:11391701 | pubmed:author | pubmed-author:NakamizoTT | lld:pubmed |
| pubmed-article:11391701 | pubmed:copyrightInfo | Copyright 2001 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:11391701 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11391701 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11391701 | pubmed:volume | 64 | lld:pubmed |
| pubmed-article:11391701 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11391701 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11391701 | pubmed:pagination | 466-75 | lld:pubmed |
| pubmed-article:11391701 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:11391701 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11391701 | pubmed:articleTitle | Nongenomic antiapoptotic signal transduction by estrogen in cultured cortical neurons. | lld:pubmed |
| pubmed-article:11391701 | pubmed:affiliation | Department of Neurology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawaharacho, Sakyo-ku, Kyoto 606-8507, Japan. | lld:pubmed |
| pubmed-article:11391701 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11391701 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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