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  会員専用

• ホーム
• 52巻11号
• 臨床神経, 52：904−907, 2012
• 52巻11号目次

＜シンポジウム（1）―1―1＞脳卒中：脳保護研究の現状と展望（Neuroprotection-Update）

脳虚血耐性現象への転写因子CREB活性化の関与

北川　一夫, 佐々木　勉, 寺崎　泰和, 八木田　佳樹, 望月　秀樹

大阪大学大学院医学系研究科神経内科学〔〒565―0871 吹田市山田丘2―2〕

Ischemic tolerance is as powerful and reproducible for neuro-protection as hypothermia. Several pathways could be involved in acquisition of ischemic tolerance. CREB is an abundant transcription factor in the brain and plays critical role on synaptic plasticity and neuronal survival. CREB activation has been also shown to be involved in ischemic tolerance. Ischemia or oxygen-glucose deprivation leads to release of glutamate, which binds to synaptic NMDA receptor. Then, influx of calcium ions into intracellular space activates calcium-calmodulin dependent protein kinase (CaMK). CaMK I/IV phosphorylates Ser 133 of CREB, and Thr 484 of salt-inducible kinase (SIK). Phosphorylation of SIK2 at Thr 484 triggers degradation of SIK2 through ubiquitin proteasome system. SIK2 maintains the phosphorylation level of CREB-regulated transcriptional co-activator (CRTC). Degradation of SIK2 induces dephosphorylation of CRTC1, and moves CRTC1 from cytoplasm into nucleus. Thus CRTC1 binds to basic ZIP domain of CREB. Both Ser133 phosphorylation and CRTC1 bound to the basic ZIP domain of CREB enhances CRE-mediated transcription, induces gene expression of survival factors, and renders the neurons resistant to subsequent severe ischemia.
Full Text of this Article in Japanese PDF (286K)

(臨床神経, 52：904−907, 2012)
key words：虚血耐性，グルタミン酸受容体，CREB特異的コアクチベータ，塩誘導性キナーゼ，選択的脆弱性

（受付日：2012年5月23日）