N-acetyl-serotonin offers neuroprotection through inhibiting mitochondrial death pathways and autophagic activation in experimental models of ischemic injury. (Q37594138)

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scientific article published on February 2014

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English	N-acetyl-serotonin offers neuroprotection through inhibiting mitochondrial death pathways and autophagic activation in experimental models of ischemic injury.	scientific article published on February 2014

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8 March 2020

N-acetyl-serotonin offers neuroprotection through inhibiting mitochondrial death pathways and autophagic activation in experimental models of ischemic injury (English)

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8 March 2020

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N-acetylserotonin

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ChEBI release 2020-05-28

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7

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8 March 2020

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8 March 2020

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Hua Zhou

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8 March 2020

Jian Wang

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8 March 2020

Jiying Jiang

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8 March 2020

Irina G Stavrovskaya

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8 March 2020

Mingchang Li

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Wei Li

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Xinmu Zhang

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Chengliang Luo

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Shuanhu Zhou

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Ana C Sirianni

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Bruce S Kristal

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Robert M Friedlander

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Xin Wang

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1 February 2014

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8 March 2020

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Journal of Neuroscience

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8 March 2020

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8 March 2020

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8 March 2020

2967-2978

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8 March 2020

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11 June 2022

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Therapeutic neuroprotective agents for amyotrophic lateral sclerosis

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23 August 2017

Inhibition of autophagy contributes to ischemic postconditioning-induced neuroprotection against focal cerebral ischemia in rats

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Retracted: Propofol Prevents Autophagic Cell Death following Oxygen and Glucose Deprivation in PC12 Cells and Cerebral Ischemia-Reperfusion Injury in Rats

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Excessive autophagy contributes to neuron death in cerebral ischemia

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N-acetylserotonin activates TrkB receptor in a circadian rhythm

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Methazolamide and melatonin inhibit mitochondrial cytochrome C release and are neuroprotective in experimental models of ischemic injury

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Neuronal injury in rat model of permanent focal cerebral ischemia is associated with activation of autophagic and lysosomal pathways

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Endonuclease G is an apoptotic DNase when released from mitochondria

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Cytochrome c release and caspase activation in traumatic axonal injury

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Mitochondria and apoptosis

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10.1523/JNEUROSCI.1948-13.2014

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8 March 2020

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8 March 2020

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8 March 2020

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