| pubmed-article:12917327 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C0149784 | lld:lifeskim |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C0023870 | lld:lifeskim |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C0244989 | lld:lifeskim |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
| pubmed-article:12917327 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
| pubmed-article:12917327 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:12917327 | pubmed:dateCreated | 2003-8-14 | lld:pubmed |
| pubmed-article:12917327 | pubmed:abstractText | Lithium has been used as an effective mood-stabilizing drug for the treatment of manic episodes and depression for 50 years. More recently, lithium has been found to protect neurons from death induced by a wide array of neurotoxic insults. However, the molecular basis for the prophylactic effects of lithium have remained obscure. A target of lithium, glycogen synthase kinase 3 (GSK-3), is implicated in neuronal death after trophic deprivation. The mechanism whereby GSK-3 exerts its neurotoxic effects is also unknown. Here we show that lithium blocks the canonical c-Jun apoptotic pathway in cerebellar granule neurons deprived of trophic support. This effect is mimicked by the structurally independent inhibitors of GSK-3, FRAT1, and indirubin. Like lithium, these prevent the stress induced c-Jun protein increase and subsequent apoptosis. These events are downstream of c-Jun transactivation, since GSK-3 inhibitors block neuronal death induced by constitutively active c-Jun (Ser/Thr-->Asp) and FRAT1 expression inhibits AP1 reporter activity. Consistent with this, AP1-dependent expression of proapoptotic Bim requires GSK-3-like activity. These data suggest that a GSK-3-like kinase acts in tandem with c-Jun N-terminal kinase to coordinate the full execution of the c-Jun stress response and neuronal death in response to trophic deprivation. | lld:pubmed |
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| pubmed-article:12917327 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12917327 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12917327 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12917327 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12917327 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12917327 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:12917327 | pubmed:author | pubmed-author:CourtneyMicha... | lld:pubmed |
| pubmed-article:12917327 | pubmed:author | pubmed-author:CoffeyEleanor... | lld:pubmed |
| pubmed-article:12917327 | pubmed:author | pubmed-author:HongistoVesaV | lld:pubmed |
| pubmed-article:12917327 | pubmed:author | pubmed-author:BrechtStephan... | lld:pubmed |
| pubmed-article:12917327 | pubmed:author | pubmed-author:HerdegenThoma... | lld:pubmed |
| pubmed-article:12917327 | pubmed:author | pubmed-author:SmedsNinaN | lld:pubmed |
| pubmed-article:12917327 | pubmed:issnType | Print | lld:pubmed |
