GADD34 induces cell death through inactivation of Akt following traumatic brain injury.
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Role of Microvascular Disruption in Brain Damage from Traumatic Brain InjuryLinking traumatic brain injury to chronic traumatic encephalopathy: identification of potential mechanisms leading to neurofibrillary tangle developmentEssential role of eIF5-mimic protein in animal development is linked to control of ATF4 expressionAltering endoplasmic reticulum stress in a model of blast-induced traumatic brain injury controls cellular fate and ameliorates neuropsychiatric symptoms.Coordinated Regulation of the Neutral Amino Acid Transporter SNAT2 and the Protein Phosphatase Subunit GADD34 Promotes Adaptation to Increased Extracellular Osmolarity.Salubrinal-Mediated Upregulation of eIF2α Phosphorylation Increases Doxorubicin Sensitivity in MCF-7/ADR Cells.Arctigenin Treatment Protects against Brain Damage through an Anti-Inflammatory and Anti-Apoptotic Mechanism after Needle InsertionmiR-711 upregulation induces neuronal cell death after traumatic brain injury.Activation of SK2 channels preserves ER Ca²⁺ homeostasis and protects against ER stress-induced cell death.The integrated stress response.Induction of GADD34 Regulates the Neurotoxicity of Amyloid β.White matter damage after traumatic brain injury: A role for damage associated molecular patterns.Calcineurin β protects brain after injury by activating the unfolded protein response.Traumatic Brain Injury Induces Alterations in Cortical Glutamate Uptake without a Reduction in Glutamate Transporter-1 Protein Expression.Targeting protein homeostasis with nelfinavir/salinomycin dual therapy effectively induces death of mTORC1 hyperactive cells.Salubrinal reduces oxidative stress, neuroinflammation and impulsive-like behavior in a rodent model of traumatic brain injury.Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it's role in metabolic defects and neuronal apoptosis after TBI.Treatment with an activator of hypoxia-inducible factor 1, DMOG provides neuroprotection after traumatic brain injury.Growth arrest and DNA damage-inducible protein (GADD34) enhanced liver inflammation and tumorigenesis in a diethylnitrosamine (DEN)-treated murine model.Isoflurane-induced inactivation of CREB through histone deacetylase 4 is responsible for cognitive impairment in developing brain.MCC950, the selective NLRP3 inflammasome inhibitor protects mice against traumatic brain injury.Activation of PERK Elicits Memory Impairment through Inactivation of CREB and Downregulation of PSD95 After Traumatic Brain Injury.Guanabenz promotes neuronal survival via enhancement of ATF4 and parkin expression in models of Parkinson disease.Translational attenuation and retinal degeneration in mice with an active integrated stress response.
P2860
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P2860
GADD34 induces cell death through inactivation of Akt following traumatic brain injury.
description
2013 nî lūn-bûn
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2013年の論文
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2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
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2013年论文
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2013年论文
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name
GADD34 induces cell death through inactivation of Akt following traumatic brain injury.
@en
type
label
GADD34 induces cell death through inactivation of Akt following traumatic brain injury.
@en
prefLabel
GADD34 induces cell death through inactivation of Akt following traumatic brain injury.
@en
P2093
P2860
P356
P1476
GADD34 induces cell death through inactivation of Akt following traumatic brain injury.
@en
P2093
J M Farook
K M Dhandapani
P2860
P356
10.1038/CDDIS.2013.280
P50
P577
2013-08-01T00:00:00Z