Regulation of neuronal cdc20 (p55cdc) expression by the plasticity-related transcription factor Zif268
Regulation of neuronal cdc20 (p55cdc) expression by the plasticity-related transcription factor Zif268
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DOI：
10.1002/syn.20387
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发表时间：
2007-06-01
期刊：
影响因子：
2.3
通讯作者：
Morris, Brian J.
中科院分区：
文献类型：
--
作者：
Conway, Ann-Marie;James, Allan B.;Morris, Brian J.
大多数形式的神经元可塑性与转录因子Zif268(Egr1)的诱导有关。在用Zif268转染神经细胞系后，观察到CDC20(P55(CDC))的下调--CDC20是后期促进复合体的调节蛋白，控制特定底物对蛋白酶体的访问。用NMDA处理培养的海马神经元，提高内源性Zif268的水平，也降低CDC20的水平。相反，与野生型对照相比，定向缺失Zif268基因的小鼠大脑皮层中CDC20的水平被发现增加。我们的研究结果表明，Zif268下调了神经细胞中CDC20基因的表达，并提供了新的证据，表明Zif268诱导后蛋白酶体调节基因的表达变化可能是中枢神经系统长期可塑性的关键组成部分。
Most forms of neuronal plasticity are associated with induction of the transcription factor zif268 (egr1). Down-regulation of cdc20 (p55(cdc))-a regulatory protein for the anaphase-promoting complex, which controls access of specific substrates to the proteasome-was observed after transfection of a neuronal cell line with zif268. Treatment of cultured hippocampal neurones with NMDA, which elevates endogenous zif268 levels, also decreased cdc20 levels. Conversely, the levels of cdc20 were found to be increased in the cerebral cortex of mice with targeted deletion of the zif268 gene, when compared with wild-type controls. Our findings indicate that expression of the cdc20 gene is down-regulated by zif268 in neuronal cells, and provide new evidence that altered expression of proteasome-regulatory genes following zif268 induction may be a key component of long-lasting CNS plasticity.