Necrostatin-1 reduces histopathology and improves functional outcome after controlled cortical impact in mice. - Wikidata - wikimedia - TriplyDB

Necrostatin-1 reduces histopathology and improves functional outcome after controlled cortical impact in mice.

Necrostatin-1 reduces histopathology and improves functional outcome after controlled cortical impact in mice.

http://www.wikidata.org/entity/Q39365993

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Endoplasmic reticulum protein BI-1 modulates unfolded protein response signaling and protects against stroke and traumatic brain injury An outline of necrosome triggers Neuroprotection for traumatic brain injury Photoreceptor cell death and rescue in retinal detachment and degenerations Biomarkers and molecular probes for cell death imaging and targeted therapeutics Role of necroptosis in the pathogenesis of solid organ injury The role of necroptosis in neurosurgical diseases Emerging therapies in traumatic brain injury Molecular mechanisms of cognitive dysfunction following traumatic brain injury The potential for bio-mediators and biomarkers in pediatric traumatic brain injury and neurocritical care RIP1-dependent and independent effects of necrostatin-1 in necrosis and T cell activation Immediate, but not delayed, microsurgical skull reconstruction exacerbates brain damage in experimental traumatic brain injury model The far-reaching scope of neuroinflammation after traumatic brain injury.5-Aminolevulinic Acid-Mediated Sonodynamic Therapy Inhibits RIPK1/RIPK3-Dependent Necroptosis in THP-1-Derived Foam Cells.Cellular stress responses: cell survival and cell death Molecular and cellular mechanisms responsible for cellular stress and low-grade inflammation induced by a super-low dose of endotoxin Retinal ganglion cell (RGC) programmed necrosis contributes to ischemia-reperfusion-induced retinal damage.Necroptosis mediates TNF-induced toxicity of hippocampal neurons.Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro.Perispinal etanercept for post-stroke neurological and cognitive dysfunction: scientific rationale and current evidence Low-level laser light therapy improves cognitive deficits and inhibits microglial activation after controlled cortical impact in mice Molecular changes and vision loss in a mouse model of closed-globe blast trauma Necroptosis RIP1 kinase mediates arachidonic acid-induced oxidative death of oligodendrocyte precursors.Genetic analysis of the role of tumor necrosis factor receptors in functional outcome after traumatic brain injury in mice.Role of Akt and mammalian target of rapamycin in functional outcome after concussive brain injury in mice The complex interplay between autophagy, apoptosis, and necrotic signals promotes T-cell homeostasis.The cystine/glutamate antiporter system x(c)(-) in health and disease: from molecular mechanisms to novel therapeutic opportunities.Activation of autophagy in photoreceptor necroptosis after experimental retinal detachment.Receptor interacting protein kinases mediate retinal detachment-induced photoreceptor necrosis and compensate for inhibition of apoptosis.Akt Regulates TNFα synthesis downstream of RIP1 kinase activation during necroptosis.Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.RIP kinases: key decision makers in cell death and innate immunity.Gene-specific differential response to anti-apoptotic therapies in zebrafish models of ocular coloboma.Neuronal deletion of caspase 8 protects against brain injury in mouse models of controlled cortical impact and kainic acid-induced excitotoxicity Cell death signalling mechanisms in heart failure.Rate of neurodegeneration in the mouse controlled cortical impact model is influenced by impactor tip shape: implications for mechanistic and therapeutic studies.Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death.Using Small Molecules to Dissect Non-apoptotic Programmed Cell Death: Necroptosis, Ferroptosis, and Pyroptosis.

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P2860

Necrostatin-1 reduces histopathology and improves functional outcome after controlled cortical impact in mice.

http://www.wikidata.org/entity/Q39365993

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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name

Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

@en

Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

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type

label

Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

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Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

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Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

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Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

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Journal of Cerebral Blood Flow & Metabolism

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Necrostatin-1 reduces histopat ...... olled cortical impact in mice.

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Gregory D Cuny

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Jinsheng Yang

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Junying Yuan

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Michael A Moskowitz

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Michael J Whalen

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Sean I Savitz

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Zerong You

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P2860

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

Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury.

Tumor necrosis factor receptor 1 and its signaling intermediates are recruited to lipid rafts in the traumatized brain

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

Colchicine induces apoptosis in organotypic hippocampal slice cultures.

Apoptotic and necrotic cell death induced by death domain receptors.

Necrotic death pathway in Fas receptor signaling

Structure-activity relationship study of tricyclic necroptosis inhibitors.

More than one way to die: methods to determine TNF-induced apoptosis and necrosis.

Inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor.

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