Aβ(1-42)-induced JNK and ERK activation in rabbit hippocampus is differentially regulated by lithium but is not involved in the phosphorylation of tau
Aβ(1-42)-induced JNK and ERK activation in rabbit hippocampus is differentially regulated by lithium but is not involved in the phosphorylation of tau
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DOI：
10.1016/j.molbrainres.2003.09.001
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发表时间：
2003-11-26
期刊：
影响因子：
--
通讯作者：
Savory, J
中科院分区：
文献类型：
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作者：
Ghribi, O;Prammonjago, P;Savory, J
将Abeta（1-42）施用到兔脑中诱导tau的凋亡和磷酸化。这些Abeta效应与JNK和ERK的激活相关，但与p38无关。用7 mM锂处理抑制细胞凋亡，调节JNK和ERK，并且不影响tau的磷酸化。我们的研究结果表明，锂，在这个剂量下，有效地抑制Abeta诱导的细胞凋亡，但对tau蛋白磷酸化没有影响，并且MAP激酶不参与tau蛋白的磷酸化。(C)2003 Elsevier B. V.保留所有权利。
Administration of Abeta(1-42) into the rabbit brain induces apoptosis and phosphorylation of tau. These Abeta effects correlate with the activation of JNK and ERK, but not of p38. Treatment with 7 mM lithium inhibits apoptosis, modulates JNK and ERK and does not affect the phosphorylation of tau. Our results demonstrate that lithium, at this dose, effectively inhibits the Abeta-induced apoptosis but has no effect on tau phosphorylation, and that MAP kinases are not involved in the phosphorylation of tau. (C) 2003 Elsevier B.V. All rights reserved.