Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain
about
Mitochondrial function in hypoxic ischemic injury and influence of agingSurvivin Is a transcriptional target of STAT3 critical to estradiol neuroprotection in global ischemiaZinc wave during the treatment of hypoxia is required for initial reactive oxygen species activation in mitochondriaERK signaling leads to mitochondrial dysfunction in extracellular zinc-induced neurotoxicity.Voltage-dependent inwardly rectifying potassium conductance in the outer membrane of neuronal mitochondria.TPEN, a Specific Zn2+ Chelator, Inhibits Sodium Dithionite and Glucose Deprivation (SDGD)-Induced Neuronal Death by Modulating Apoptosis, Glutamate Signaling, and Voltage-Gated K+ and Na+ Channels.The mitochondrial complex V-associated large-conductance inner membrane current is regulated by cyclosporine and dexpramipexoleZn²+ chelation improves recovery by delaying spreading depression-like events.Mechanisms of rapid reactive oxygen species generation in response to cytosolic Ca2+ or Zn2+ loads in cortical neurons.The neurophysiology and pathology of brain zinc.Intracellular zinc release, 12-lipoxygenase activation and MAPK dependent neuronal and oligodendroglial death.Reduction of zinc accumulation in mitochondria contributes to decreased cerebral ischemic injury by normobaric hyperoxia treatment in an experimental stroke model.Ischemic preconditioning blocks BAD translocation, Bcl-xL cleavage, and large channel activity in mitochondria of postischemic hippocampal neurons.Heavy metal ions in normal physiology, toxic stress, and cytoprotection.The role of zinc in cerebral ischemia.Zn2+ influx is critical for some forms of spreading depression in brain slices.Intracellular Zn2+ accumulation contributes to synaptic failure, mitochondrial depolarization, and cell death in an acute slice oxygen-glucose deprivation model of ischemia.Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currentsN-terminally cleaved Bcl-xL mediates ischemia-induced neuronal deathMolecular participants in mitochondrial cell death channel formation during neuronal ischemia.Contributions of Ca2+ and Zn2+ to spreading depression-like events and neuronal injury.Differential Vulnerability of CA1 versus CA3 Pyramidal Neurons After Ischemia: Possible Relationship to Sources of Zn2+ Accumulation and Its Entry into and Prolonged Effects on Mitochondria.The interactive roles of zinc and calcium in mitochondrial dysfunction and neurodegeneration.Zinc: new clues to diverse roles in brain ischemia.Ca permeable AMPA channels in diseases of the nervous system.Mitochondrial channels: ion fluxes and more.Regulators of mitochondrial Ca(2+) homeostasis in cerebral ischemia.Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase.Bcl-xL inhibitor ABT-737 reveals a dual role for Bcl-xL in synaptic transmission.Intramitochondrial Zn2+ accumulation via the Ca2+ uniporter contributes to acute ischemic neurodegeneration.Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency.Heat acclimation provides sustained improvement in functional recovery and attenuates apoptosis after traumatic brain injury.Cross talk between increased intracellular zinc (Zn2+) and accumulation of reactive oxygen species in chemical ischemia.Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity.Characterisation of element profile changes induced by long-term dietary supplementation of zinc in the brain and cerebellum of 3xTg-AD mice by alternated cool and normal plasma ICP-MS.Rising zinc: a significant cause of ischemic neuronal death in the CA1 region of rat hippocampus.Zn2+-induced disruption of neuronal mitochondrial function: Synergism with Ca2+, critical dependence upon cytosolic Zn2+ buffering, and contributions to neuronal injury.Multiple molecular mechanisms form a positive feedback loop driving amyloid β42 peptide-induced neurotoxicity via activation of the TRPM2 channel in hippocampal neurons.Zinc irreversibly damages major enzymes of energy production and antioxidant defense prior to mitochondrial permeability transition.The Zinc Ion Chelating Agent TPEN Attenuates Neuronal Death/apoptosis Caused by Hypoxia/ischemia Via Mediating the Pathophysiological Cascade Including Excitotoxicity, Oxidative Stress, and Inflammation.
P2860
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P2860
Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@ast
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@en
type
label
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@ast
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@en
prefLabel
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@ast
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@en
P2093
P2860
P1476
Zinc-dependent multi-conductan ...... a isolated from ischemic brain
@en
P2093
Adrienne Jones
Brian M Polster
Chang-Hoon Cho
Dimitry Ofengeim
Elizabeth A Jonas
Hidenori Yokota
Hongmei Li
J Marie Hardwick
Marc Pypaert
Mushtaque Chachar
P2860
P304
P356
10.1523/JNEUROSCI.5444-05.2006
P407
P577
2006-06-01T00:00:00Z