Increased Phosphorylation of a 17‐kDa Protein Kinase C Substrate (P17) in Long‐Term Potentiation
Increased Phosphorylation of a 17‐kDa Protein Kinase C Substrate (P17) in Long‐Term Potentiation
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长时程增强中 17-kDa 蛋白激酶 C 底物 (P17) 的磷酸化增加
DOI：
10.1111/j.1471-4159.1992.tb11382.x
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发表时间：
1992
影响因子：
4.7
通讯作者：
J. Sweatt
中科院分区：
文献类型：
--
作者：
E. Klann;Shu‐Jen Chen;J. Sweatt
海马长时程增强（hippocampus long - term potentiation， LTP）是突触传递效能的持续增强，被广泛认为是一种有助于学习和记忆的细胞机制。对LTP生化机制的研究表明，蛋白激酶参与LTP的诱导和维持。在本报告中，我们描述了在大鼠海马切片CA1区域的均质液中，与LTP相关的17 - kDa蛋白激酶C （PKC）底物蛋白（我们称之为P17）的体外磷酸化增加。当磷酸化反应在500 μM EGTA存在下进行时，LTP相关的磷酸化增加的表达与显著水平的游离Ca2+无关。P17磷酸化的增加被PKC（一种PKC的选择性抑制剂）显著抑制（19-36）。这些数据支持了PKC持续激活有助于LTP维持的模型，并暗示P17是海马CA1区PKC的潜在靶点。
Abstract: Hippocampal long‐term potentiation (LTP) is a persistent increase in the efficacy of synaptic transmission, which is widely thought to be a cellular mechanism that could contribute to learning and memory. Studies on the biochemical mechanisms underlying LTP suggest the involvement of protein kinases in both LTP induction and maintenance. In this report we describe an LTP‐associated increase in the phosphorylation in vitro of a 17‐kDa protein kinase C (PKC) substrate protein, which we have termed P17, in homogenates from the CA1 region of rat hippocampal slices. This LTP‐associated increase in phosphorylation was expressed independent of significant levels of free Ca2+, as phosphorylation reactions were performed in the presence of 500 μM EGTA. The increased phosphorylation of P17 was substantially inhibited by PKC(19–36), a selective inhibitor of PKC. These data support the model that persistent PKC activation contributes to the maintenance of LTP and implicate P17 as a potential target for PKC in the CA1 region of the hippocampus.
来自牛脑的蛋白激酶 C 底物。
DOI：
--
发表时间：
1989
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Baudier,J;Bronner,C;Kligman,D;Cole,RD
通讯作者：
Cole,RD
47-kDa 蛋白 (F1) 磷酸化的选择性增加与长时程增强直接相关。
DOI：
10.1016/s0163-1047(85)91426-8
发表时间：
1985
期刊：
Behavioral and neural biology
影响因子：
--
作者：
Routtenberg,A;Lovinger,DM
通讯作者：
Lovinger,DM
影响因子：
56.9
作者：
MALINOW, R;SCHULMAN, H;TSIEN, RW
通讯作者：
TSIEN, RW