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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Reduced viability of neuronal cells after overexpression of protein histidine phosphatase.
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Reduced viability of neuronal cells after overexpression of protein histidine phosphatase.

机译：蛋白组氨酸磷酸酶过表达后神经元细胞活力降低。

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Protein histidine phosphatase (PHP) has just recently been discovered in eukaryotes and ATP-citrate lyase (ACL) was shown to be one of its substrates. Since ACL is crucial for cellular energy and fat metabolism we made an attempt to study the influence of PHP on cell viability. Using an adenoviral vector PHP was overexpressed in SN56 cholinergic murine neuroblastoma cells and in primary cultures of hippocampal neurons obtained from embryonic rats (E18). Overexpression of PHP in these cells caused a decrease in ACL activity and consequently impaired viability. To be sure that the reduced cellular viability was achieved by overexpression of PHP we also downregulated ACL in SN56 cells using RNAi-technology. Downregulation of ACL was harmful to the cells similar to what was observed upon overexpression of PHP. Taken together, it is concluded that overexpression of PHP results in increased dephosphorylation with concomitant inactivation of ACL, thus finally leading to cell damage.
机译：蛋白质组氨酸磷酸酶（PHP）是最近在真核生物中发现的，ATP-柠檬酸裂解酶（ACL）被证明是其底物之一。由于ACL对于细胞能量和脂肪代谢至关重要，因此我们尝试研究PHP对细胞活力的影响。使用腺病毒载体，PHP在SN56胆碱能鼠神经母细胞瘤细胞和从胚胎大鼠获得的海马神经元的原代培养物中过度表达（E18）。这些细胞中PHP的过表达导致ACL活性降低，并因此降低了生存能力。为确保降低的细胞活力是通过PHP的过表达实现的，我们还使用RNAi技术下调了SN56细胞中的ACL。 ACL的下调对细胞有害，类似于PHP过表达时观察到的情况。两者合计，得出的结论是，PHP的过表达导致去磷酸化的增加以及ACL的失活，从而最终导致细胞损伤。

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