Autophagy is Increased after Traumatic Brain Injury in Mice and is Partially Inhibited by the Antioxidant γ-glutamylcysteinyl Ethyl Ester (Q61718225)

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English	Autophagy is Increased after Traumatic Brain Injury in Mice and is Partially Inhibited by the Antioxidant γ-glutamylcysteinyl Ethyl Ester	article

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5 January 2020

Autophagy is increased after traumatic brain injury in mice and is partially inhibited by the antioxidant gamma-glutamylcysteinyl ethyl ester (English)

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Charleen T. Chu

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Patrick M. Kochanek

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Hülya Bayir

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Robert W Hickey

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Yaming Chen

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Mara L Sullivan

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C Edward Dixon

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Larry W Jenkins

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Steven H Graham

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Simon C Watkins

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Robert S B Clark

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5 September 2007

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Journal of Cerebral Blood Flow & Metabolism

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540-550

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5 January 2020

Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 1: Introduction.

1 reference

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Cerebral ischemia-hypoxia induces intravascular coagulation and autophagy

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Neuronal macroautophagy: from development to degeneration

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Autophagic stress in neuronal injury and disease.

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boc-Aspartyl(OMe)-fluoromethylketone attenuates mitochondrial release of cytochrome c and delays brain tissue loss after traumatic brain injury in rats.

1 reference

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Closed head injury induces upregulation of Beclin 1 at the cortical site of injury.

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Elevation of brain glutathione by gamma-glutamylcysteine ethyl ester protects against peroxynitrite-induced oxidative stress

1 reference

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Elevation of mitochondrial glutathione by gamma-glutamylcysteine ethyl ester protects mitochondria against peroxynitrite-induced oxidative stress

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The effect of postinjury administration of polyethylene glycol-conjugated superoxide dismutase (pegorgotein, Dismutec) or lidocaine on behavioral function following fluid-percussion brain injury in rats

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Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

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Biogenesis of multilamellar bodies via autophagy

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A ubiquitin-like system mediates protein lipidation

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The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia

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Participation of autophagy in storage of lysosomes in neurons from mouse models of neuronal ceroid-lipofuscinoses (Batten disease).

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Loss of autophagy in the central nervous system causes neurodegeneration in mice

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Attenuation of acute and chronic damage following traumatic brain injury in copper, zinc-superoxide dismutase transgenic mice.

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Intracellular quality control by autophagy: how does autophagy prevent neurodegeneration?

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In vivo analysis of autophagy in response to nutrient starvation using transgenic mice expressing a fluorescent autophagosome marker

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Methods for monitoring autophagy

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Localization of products of endogenous proteolysis in lysosomes of perfused rat liver.

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Extensive involvement of autophagy in Alzheimer disease: an immuno-electron microscopy study.

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A dual role for poly‐ADP‐ribosylation in spatial memory acquisition after traumatic brain injury in mice involving NAD+ depletion and ribosylation of 14‐3‐3γ

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Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4

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3-Methyladenine: specific inhibitor of autophagic/lysosomal protein degradation in isolated rat hepatocytes

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HsAtg4B/HsApg4B/autophagin-1 cleaves the carboxyl termini of three human Atg8 homologues and delipidates microtubule-associated protein light chain 3- and GABAA receptor-associated protein-phospholipid conjugates

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Oxidative stress following traumatic brain injury in rats: quantitation of biomarkers and detection of free radical intermediates

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Induction of autophagy in axonal dystrophy and degeneration

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Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor

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10.1038/SJ.JCBFM.9600551

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