Role of mitogen- and stress-activated kinases in ischemic injury. - Wikidata - wikimedia - TriplyDB

Role of mitogen- and stress-activated kinases in ischemic injury.

Role of mitogen- and stress-activated kinases in ischemic injury.

http://www.wikidata.org/entity/Q34667918

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Neuroprotection for ischemic stroke: past, present and future Role of redox signaling in neuroinflammation and neurodegenerative diseases Cell-permeable p38 MAP kinase promotes migration of adult neural stem/progenitor cells.Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia Mitochondrial function in hypoxic ischemic injury and influence of aging ROS detoxification and proinflammatory cytokines are linked by p38 MAPK signaling in a model of mature astrocyte activation Cabergoline, dopamine D2 receptor agonist, prevents neuronal cell death under oxidative stress via reducing excitotoxicity Critical role of PTEN in the coupling between PI3K/Akt and JNK1/2 signaling in ischemic brain injury Interaction of ARC and Daxx: A Novel Endogenous Target to Preserve Motor Function and Cell Loss after Focal Brain Ischemia in Mice Glutamate transporter type 3 mediates isoflurane preconditioning-induced acute phase of neuroprotection in mice Transient focal cerebral ischemia induces long-term cognitive function deficit in an experimental ischemic stroke model.Putative endogenous mediators of preconditioning-induced ischemic tolerance in rat brain identified by genomic and proteomic analysis.Neuroprotection provided by isoflurane pre-conditioning and post-conditioning Multifaceted Mechanisms of WY-14643 to Stabilize the Blood-Brain Barrier in a Model of Traumatic Brain Injury Upregulation of glutamate metabolism by BYHWD in cultured astrocytes following oxygen-glucose deprivation/reoxygenation in part depends on the activation of p38 MAPK.A novel dual NO-donating oxime and c-Jun N-terminal kinase inhibitor protects against cerebral ischemia-reperfusion injury in mice Innate inflammatory responses in stroke: mechanisms and potential therapeutic targets.JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury Phosphorylation of HSP27 by protein kinase D is essential for mediating neuroprotection against ischemic neuronal injury.Thrombin-induced neuronal protection: role of the mitogen activated protein kinase/ribosomal protein S6 kinase pathway.Neuroprotective effects of bilobalide on cerebral ischemia and reperfusion injury are associated with inhibition of pro-inflammatory mediator production and down-regulation of JNK1/2 and p38 MAPK activation.A critical role of neural-specific JNK3 for ischemic apoptosis.MAPK signaling pathway regulates cerebrovascular receptor expression in human cerebral arteries.Cell cycle molecules define a pathway required for neuron death in development and disease.Mitogen-activated protein kinases in the porcine retinal arteries and neuroretina following retinal ischemia-reperfusion.Oxidative stress in ischemic brain damage: mechanisms of cell death and potential molecular targets for neuroprotection Enriched environment prevents hypobaric hypoxia induced memory impairment and neurodegeneration: role of BDNF/PI3K/GSK3β pathway coupled with CREB activation.Signal transducers and activators of transcription: STATs-mediated mitochondrial neuroprotection Heat-shock protein 90 alpha (HSP90α) modulates signaling pathways towards tolerance of oxidative stress and enhanced survival of hepatocytes of Mugil cephalus.Anti-parkinsonian effects of octacosanol in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-treated mice.Ketamine inhibits c-Jun protein expression in mouse hippocampus following cerebral ischemia/reperfusion injury.Acute inhibition of TAK1 protects against neuronal death in cerebral ischemia.Neuroprotective effects of DAHP and Triptolide in focal cerebral ischemia via apoptosis inhibition and PI3K/Akt/mTOR pathway activation.Cdk5 Modulation of mitogen-activated protein kinase signaling regulates neuronal survival.Oxidative neuronal injury. The dark side of ERK1/2.Ischemia-induced stimulation of cerebral microvascular endothelial cell Na-K-Cl cotransport involves p38 and JNK MAP kinases.The cytokine tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 have a neuroprotective effect in the central nervous system.Prokineticin 2 is an endangering mediator of cerebral ischemic injury Csk-Induced Phosphorylation of Src at Tyrosine 530 is Essential for H2O2-Mediated Suppression of ERK1/2 in Human Umbilical Vein Endothelial Cells.Heme oxygenase 1 induction protects myocardiac cells against hypoxia/reoxygenation-induced apoptosis : The role of JNK/c-Jun/Caspase-3 inhibition and Akt signaling enhancement.

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Role of mitogen- and stress-activated kinases in ischemic injury.

http://www.wikidata.org/entity/Q34667918

description

2002 nî lūn-bûn

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2002 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2002 թվականի հունիսին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Role of mitogen- and stress-activated kinases in ischemic injury.

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Role of mitogen- and stress-activated kinases in ischemic injury.

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Role of mitogen- and stress-activated kinases in ischemic injury.

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type

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Role of mitogen- and stress-activated kinases in ischemic injury.

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Role of mitogen- and stress-activated kinases in ischemic injury.

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Role of mitogen- and stress-activated kinases in ischemic injury.

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prefLabel

Role of mitogen- and stress-activated kinases in ischemic injury.

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Role of mitogen- and stress-activated kinases in ischemic injury.

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Role of mitogen- and stress-activated kinases in ischemic injury.

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Journal of Cerebral Blood Flow & Metabolism

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Role of mitogen- and stress-activated kinases in ischemic injury.

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P2093

Elaine A Irving

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Mark Bamford

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P2860

ERKs: a family of protein-serine/threonine kinases that are activated and tyrosine phosphorylated in response to insulin and NGF

A protein kinase involved in the regulation of inflammatory cytokine biosynthesis

Mitogen- and stress-activated protein kinase-1 (MSK1) is directly activated by MAPK and SAPK2/p38, and may mediate activation of CREB

MNK1, a new MAP kinase-activated protein kinase, isolated by a novel expression screening method for identifying protein kinase substrates

Convergence of MAP kinase pathways on the ternary complex factor Sap-1a.

Specificity of receptor tyrosine kinase signaling: transient versus sustained extracellular signal-regulated kinase activation

Signaling through scaffold, anchoring, and adaptor proteins

Pro-inflammatory cytokines and environmental stress cause p38 mitogen-activated protein kinase activation by dual phosphorylation on tyrosine and threonine

MEK kinase activity is not necessary for Raf-1 function.

Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo

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