Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI. - Wikidata - awgldk - TriplyDB

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

http://www.wikidata.org/entity/Q34627513

about

Many stimuli pull the necrotic trigger, an overview Fueling the flames: Mammalian programmed necrosis in inflammatory diseases Biomarkers and molecular probes for cell death imaging and targeted therapeutics The mechanism of necroptosis in normal and cancer cells Role of necroptosis in the pathogenesis of solid organ injury New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases Programmed necrosis in the cross talk of cell death and inflammation Role of mitochondria in apoptotic and necroptotic cell death in the developing brain 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy Inhibits RIPK1/RIPK3-Dependent Necroptosis in THP-1-Derived Foam Cells.Pathophysiology of glia in perinatal white matter injury.Necrostatin-1 attenuates mitochondrial dysfunction in neurons and astrocytes following neonatal hypoxia-ischemia.Mitochondrial dysfunction induces Sarm1-dependent cell death in sensory neurons Necroptosis Cell death signalling mechanisms in heart failure.Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death.Upregulation of the receptor-interacting protein 3 expression and involvement in neural tissue damage after spinal cord injury in mice.NO donor induces Nec-1-inhibitable, but RIP1-independent, necrotic cell death in pancreatic β-cells.Past, present, and future of molecular and cellular oncology Programmed Necrosis: A Prominent Mechanism of Cell Death following Neonatal Brain Injury Receptor Interacting Protein 3-Mediated Necroptosis Promotes Lipopolysaccharide-Induced Inflammation and Acute Respiratory Distress Syndrome in Mice.Dichotomy between RIP1- and RIP3-mediated necroptosis in tumor necrosis factor-α-induced shock.Pathophysiology of perinatal asphyxia: can we predict and improve individual outcomes?Sex differences in cell genesis, hippocampal volume and behavioral outcomes in a rat model of neonatal HI Endoplasmic reticulum pathology and stress response in neurons precede programmed necrosis after neonatal hypoxia-ischemia.Necroptosis, a novel type of programmed cell death, contributes to early neural cells damage after spinal cord injury in adult mice.Necrostatin-1 analogues: critical issues on the specificity, activity and in vivo use in experimental disease models Absence of receptor interacting protein kinase 3 prevents ethanol-induced liver injury Perinatal brain damage: The term infant.Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury Caspase blockade induces RIP3-mediated programmed necrosis in Toll-like receptor-activated microglia.Increased hepatic receptor interacting protein kinase 3 expression due to impaired proteasomal functions contributes to alcohol-induced steatosis and liver injury.Treatment advances in neonatal neuroprotection and neurointensive care.Structural basis of signal transduction in the TNF receptor superfamily Protective effects of necrostatin-1 against concanavalin A-induced acute hepatic injury in mice Vitamin C induces apoptosis in AGS cells via production of ROS of mitochondria.The rodent endovascular puncture model of subarachnoid hemorrhage: mechanisms of brain damage and therapeutic strategies.True grit: programmed necrosis in antiviral host defense, inflammation, and immunogenicity.Akt and mTOR mediate programmed necrosis in neurons.Sexual dimorphism in BDNF signaling after neonatal hypoxia-ischemia and treatment with necrostatin-1.Necrosis-dependent and independent signaling of the RIP kinases in inflammation.

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P2860

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

http://www.wikidata.org/entity/Q34627513

description

2010 nî lūn-bûn

@nan

2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@ast

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@en

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

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type

label

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@ast

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@en

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@nl

prefLabel

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@ast

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@en

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@nl

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P1433

Journal of Cerebral Blood Flow & Metabolism

P1476

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

@en

P2093

Ernest M Graham

http://www.w3.org/2001/XMLSchema#string

Estelle B Gauda

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Frances J Northington

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Lee J Martin

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P2860

Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule

Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation

A new mathematical model for relative quantification in real-time RT-PCR

RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis

Identification of RIP1 kinase as a specific cellular target of necrostatins

Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury

The death domain kinase RIP mediates the TNF-induced NF-kappaB signal

Nitration of the mitochondrial complex I subunit NDUFB8 elicits RIP1- and RIP3-mediated necrosis

The cardioprotective effect of necrostatin requires the cyclophilin-D component of the mitochondrial permeability transition pore

Delayed neurodegeneration in neonatal rat thalamus after hypoxia-ischemia is apoptosis.

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178-189

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10.1038/JCBFM.2010.72

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1

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31

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Raul Chavez-Valdez

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44695877

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20571523

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3049482

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