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Hyperosmotic stress-induced ATF-2 activation through Polo-like kinase 3 in human corneal epithelial cellsp38 activation is required upstream of potassium current enhancement and caspase cleavage in thiol oxidant-induced neuronal apoptosisIncreased anion channel activity is an unavoidable event in ozone-induced programmed cell deathRole of AQP2 during apoptosis in cortical collecting duct cellsTASK1 modulates inflammation and neurodegeneration in autoimmune inflammation of the central nervous system.Neuropeptides bombesin and calcitonin inhibit apoptosis-related elemental changes in prostate carcinoma cell lines.Therapeutic targets and limits of minocycline neuroprotection in experimental ischemic stroke.Tetramerization domain mutations in KCNA5 affect channel kinetics and cause abnormal trafficking patterns.Effect of minocycline on cerebral ischemia-reperfusion injuryApoptosis repressor with caspase domain inhibits cardiomyocyte apoptosis by reducing K+ currents.Inhibition of Na+/K+-ATPase induces hybrid cell death and enhanced sensitivity to chemotherapy in human glioblastoma cells.Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration.Osmotic stress-induced phosphorylation of H2AX by polo-like kinase 3 affects cell cycle progression in human corneal epithelial cellsA method for estimating intracellular sodium concentration and extracellular volume fraction in brain in vivo using sodium magnetic resonance imagingNeuropathology in Drosophila membrane excitability mutantsPost-transcriptional regulation of GORK channels by superoxide anion contributes to increases in outward-rectifying K⁺ currents.An S-type anion channel SLAC1 is involved in cryptogein-induced ion fluxes and modulates hypersensitive responses in tobacco BY-2 cells.Hyperosmotic stress-induced corneal epithelial cell death through activation of Polo-like kinase 3 and c-Jun.Repeatability of quantitative sodium magnetic resonance imaging for estimating pseudo-intracellular sodium concentration and pseudo-extracellular volume fraction in brain at 3 TFunctional ion channels in human pulmonary artery smooth muscle cells: Voltage-dependent cation channels.Long-lasting intrinsic optical changes observed in the neurointermediate lobe of the mouse pituitary reflect volume changes in cells of the pars intermedia.Activation of the low molecular weight protein tyrosine phosphatase in keratinocytes exposed to hyperosmotic stressActivation of K+ channels: an essential pathway in programmed cell death.Stress-induced corneal epithelial apoptosis mediated by K+ channel activationSafety profile of solid lipid nanoparticles loaded with rosmarinic acid for oral use: in vitro and animal approachesWater and ion channels: crucial in the initiation and progression of apoptosis in central nervous system?Cationic gradient reversal and cytoskeleton-independent volume regulatory pathways define an early stage of apoptosis.A novel channelopathy in pulmonary arterial hypertension.Apoptotic Volume Decrease (AVD) Is Independent of Mitochondrial Dysfunction and Initiator Caspase Activation.Synchrotron X-ray fluorescence studies of a bromine-labelled cyclic RGD peptide interacting with individual tumor cells.Apoptotic volume decrease as a geometric determinant for cell dismantling into apoptotic bodies.Ion channels in autoimmune neurodegeneration.Cross-talk between reactive oxygen species and polyamines in regulation of ion transport across the plasma membrane: implications for plant adaptive responses.Ozone-induced caspase-like activities are dependent on early ion channel regulations and ROS generation in Arabidopsis thaliana cells.Perturbation of intracellular K(+) homeostasis with valinomycin promotes cell death by mitochondrial swelling and autophagic processes.Pancreatic β-cell prosurvival effects of the incretin hormones involve post-translational modification of Kv2.1 delayed rectifier channels.Overexpression of mouse IsK protein fused to green fluorescent protein induces apoptosis of human astroglioma cells.Characterization of large-conductance Ca2+-dependent and -independent K+ channels in HaCaT keratinocytes.A large conductance [Ca(2+)](i)-independent K(+) channel expressed in HaCaT keratinocytes.G-Protein-Coupled Inwardly Rectifying Potassium (GIRK) Channel Activation by the p75 Neurotrophin Receptor Is Required for Amyloid β Toxicity.
P2860
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P2860
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Ions, cell volume, and apoptosis
@ast
Ions, cell volume, and apoptosis
@en
type
label
Ions, cell volume, and apoptosis
@ast
Ions, cell volume, and apoptosis
@en
prefLabel
Ions, cell volume, and apoptosis
@ast
Ions, cell volume, and apoptosis
@en
P2860
P356
P1476
Ions, cell volume, and apoptosis
@en
P2860
P304
P356
10.1073/PNAS.97.17.9360
P407
P577
2000-08-01T00:00:00Z