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Inhibition of autophagy and glycolysis by nitric oxide during hypoxia-reoxygenation impairs cellular bioenergetics and promotes cell death in primary neurons

Excessive nitric oxide (NO) production is known to damage mitochondrial proteins and the autophagy repair pathway and so can potentially contribute to neurotoxicity. Accordingly, we hypothesized that protection against protein damage from reactive oxygen and nitrogen species (ROS/RNS) under conditio...

Täydet tiedot

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Bibliografiset tiedot
Päätekijät: Benavides, Gloria A., Liang, Qiuli, Dodson, Matthew, Darley-Usmar, Victor, Zhang, Jianhua
Aineistotyyppi: Artigo
Kieli:Inglês
Julkaistu: 2013
Aiheet:
Linkit:https://ncbi.nlm.nih.gov/pmc/articles/PMC3859859/
https://ncbi.nlm.nih.gov/pubmed/24056030
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.freeradbiomed.2013.09.006
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