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短暂性全脑缺血诱导海马 CA1 神经元中 MLTKα 的上调。

Transient global cerebral ischemia induces up-regulation of MLTKα in hippocampal CA1 neurons.

机构信息

Department of Neurosurgery, Surgical Research Center, Hospital Affiliated to Nantong University, Xisi Road 20#, Nantong, 226001, Jiangsu, China.

出版信息

J Mol Histol. 2012 Apr;43(2):187-93. doi: 10.1007/s10735-011-9381-z. Epub 2011 Dec 7.

Abstract

MLTK (mixed-lineage kinase-like mitogen-activated protein triple kinase) is a member of the mitogen-activated protein kinase family and functioned as a mitogen activated kinase kinase kinase. MLTKα, one of the alternatively spliced forms of MLTK, could activate the c-Jun N-terminal kinase pathway, which involved in cellular stress responses and apoptosis. But the role of MLTKα in neural apoptosis was still unclear. Here, we performed a transient global cerebral ischemia model (TGCI) in adult rats and detected the dynamic changes of MLTKα in hippocampal CA1 neurons and brain cortex. We found the MLTKα expression was increased shortly after TGCI and peaked after 8 h. In spatial distribution, MLTKα was widely located in neurons rather than astrocytes and microglia. Moreover, there was a concomitant up-regulation of active caspase-3. Taken together, we hypothesized the up-regulation of MLTKα played an essential role in the apoptosis of hippocampal CA1 neurons.

摘要

MLTK(混合谱系激酶样丝裂原激活蛋白激酶三重激酶)是丝裂原激活蛋白激酶家族的成员,作为丝裂原激活激酶激酶起作用。MLTKα 是 MLTK 的一种选择性剪接形式,可激活 c-Jun N 端激酶途径,该途径涉及细胞应激反应和细胞凋亡。但是 MLTKα 在神经细胞凋亡中的作用尚不清楚。在这里,我们在成年大鼠中进行了短暂的全脑缺血模型(TGCI),并检测了海马 CA1 神经元和大脑皮层中 MLTKα 的动态变化。我们发现 MLTKα 的表达在 TGCI 后不久增加,并在 8 小时后达到峰值。在空间分布上,MLTKα 广泛存在于神经元中,而不是星形胶质细胞和小胶质细胞中。此外,活性半胱天冬酶-3 也随之上调。综上所述,我们假设 MLTKα 的上调在海马 CA1 神经元的凋亡中起着重要作用。

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