SAP97将Kv4.2定位至海马神经元的树突棘：受CaMKII调节。
SAP97 directs the localization of Kv4.2 to spines in hippocampal neurons: regulation by CaMKII.
作者信息
Gardoni Fabrizio, Mauceri Daniela, Marcello Elena, Sala Carlo, Di Luca Monica, Jeromin Andreas
机构信息
Department of Pharmacological Sciences and Center of Excellence on Neurodegenerative Diseases, University of Milan, via Balzaretti 9, 20133 Milan, Italy.
Cellular and Molecular Pharmacology Section, Institute of Neuroscience, Consiglio Nazionale Ricerche, and Department of Pharmacology, University of Milan, 20129 Milan, Italy.
出版信息
J Biol Chem. 2007 Sep 28;282(39):28691-28699. doi: 10.1074/jbc.M701899200. Epub 2007 Jul 16.
The pore-forming alpha-subunit Kv4.2 is a key constituent of the A-type channel and critically involved in the regulation of dendritic excitability and plasticity. Here we show that Kv4.2 is enriched in the postsynaptic density (PSD) fraction and specifically interacts with synapse-associated protein 97 (SAP97). This interaction requires an intact C terminus of Kv4.2 and occurs via the PDZ domains of SAP97. Pharmacologically induced translocation of SAP97 to spines also drives Kv4.2 to the PSD, whereas SAP97 lentivirally based RNA interference reduces Kv4.2 in the PSD. In addition, calcium/calmodulin-dependent protein kinase II (CaMKII)-dependent SAP97 phosphorylation regulates the subcellular localization of Kv4.2. These results show that SAP97-CaMKII pathway plays an important role for the trafficking of Kv4.2 to dendrites and spines.
形成孔道的α亚基Kv4.2是A类通道的关键组成部分，在树突兴奋性和可塑性的调节中起关键作用。我们在此表明，Kv4.2在突触后致密物（PSD）组分中富集，并与突触相关蛋白97（SAP97）特异性相互作用。这种相互作用需要Kv4.2完整的C末端，并且通过SAP97的PDZ结构域发生。药理学诱导的SAP97向棘突的转位也会将Kv4.2驱动到PSD，而基于慢病毒的SAP97 RNA干扰会减少PSD中的Kv4.2。此外，钙/钙调蛋白依赖性蛋白激酶II（CaMKII）依赖性的SAP97磷酸化调节Kv4.2的亚细胞定位。这些结果表明，SAP97-CaMKII途径在Kv4.2向树突和棘突的运输中起重要作用。
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