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突触结合蛋白IV存在于高尔基体和神经突的远端部分。

Synaptotagmin IV is present at the Golgi and distal parts of neurites.

作者信息

Ibata K, Fukuda M, Hamada T, Kabayama H, Mikoshiba K

机构信息

Laboratory for Developmental Neurobiology, Brain Science Institute, Institute of Physical and Chemical Research (RIKEN), Wako, Saitama, Japan.

出版信息

J Neurochem. 2000 Feb;74(2):518-26. doi: 10.1046/j.1471-4159.2000.740518.x.

Abstract

Synaptotagmin IV (SytIV) is an immediate early gene induced by membrane depolarization in PC12 cells and in rat brain. However, little is known about the function of SytIV or the functional relationship between SytIV and SytI, because SytIV has yet to be localized. Here we show that SytIV was localized at the Golgi and distal part of neurites in nerve growth factor-differentiated PC12 cells and cultured hippocampal neurons by immunocytochemistry using an isoform-specific antibody (anti-SytIV). These SytIV signals were not colocalized well with SytI signals. Upon membrane depolarization, SytIV signals were increased at both the Golgi and distal part of neurites within several hours in both types of cells. We further show that the increase of SytIV protein levels results from protein kinase A-dependent gene up-regulation. In hippocampal neurons, SytIV was developmentally regulated. These results suggest that SytIV may play a role at the Golgi and tips of neurites during development and synaptic plasticity.

摘要

突触结合蛋白IV(SytIV)是一种在PC12细胞和大鼠脑中由膜去极化诱导的即早基因。然而,由于SytIV尚未定位,对其功能或SytIV与SytI之间的功能关系了解甚少。在这里,我们通过使用同种型特异性抗体(抗SytIV)进行免疫细胞化学显示,SytIV定位于神经生长因子分化的PC12细胞和培养的海马神经元中的高尔基体和神经突的远端部分。这些SytIV信号与SytI信号的共定位不佳。在膜去极化后,两种类型的细胞在数小时内高尔基体和神经突远端部分的SytIV信号均增加。我们进一步表明,SytIV蛋白水平的增加是由蛋白激酶A依赖性基因上调引起的。在海马神经元中,SytIV受发育调控。这些结果表明,SytIV可能在发育和突触可塑性过程中在高尔基体和神经突末端发挥作用。

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