Elevation of mitochondrial transmembrane potential and reactive oxygen intermediate levels are early events and occur independently from activation of caspases in Fas signaling
about
Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activityRole of mitochondria in the pheromone- and amiodarone-induced programmed death of yeast.Mitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosusExpression of P-170 glycoprotein sensitizes lymphoblastoid CEM cells to mitochondria-mediated apoptosisMechanisms underlying production and externalization of oxidized phosphatidylserine in apoptosis: involvement of mitochondriaReactive oxygen species production and mitochondrial dysfunction contribute to quercetin induced death in Leishmania amazonensisAcrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stressParaoxonase 2 decreases renal reactive oxygen species production, lowers blood pressure, and mediates dopamine D2 receptor-induced inhibition of NADPH oxidaseTransaldolase is essential for maintenance of the mitochondrial transmembrane potential and fertility of spermatozoa.Turning up the heat: heat stress induces markers of programmed cell death in Plasmodium falciparum in vitro.A role of reactive oxygen species in apoptotic activation of volume-sensitive Cl(-) channel.Proteomic and systems biology analysis of the monocyte response to Coxiella burnetii infection.Cleavage of transaldolase by granzyme B causes the loss of enzymatic activity with retention of antigenicity for multiple sclerosis patients.Systems biology of lupus: mapping the impact of genomic and environmental factors on gene expression signatures, cellular signaling, metabolic pathways, hormonal and cytokine imbalance, and selecting targets for treatment.Persistent mitochondrial hyperpolarization, increased reactive oxygen intermediate production, and cytoplasmic alkalinization characterize altered IL-10 signaling in patients with systemic lupus erythematosus.Mitochondrial hyperpolarization: a checkpoint of T-cell life, death and autoimmunity.Nitric oxide-dependent mitochondrial biogenesis generates Ca2+ signaling profile of lupus T cells.Rapamycin reduces disease activity and normalizes T cell activation-induced calcium fluxing in patients with systemic lupus erythematosus.Oxidative stress in the pathology and treatment of systemic lupus erythematosusT-cell and B-cell signaling biomarkers and treatment targets in lupus.Increased mitochondrial electron transport chain activity at complex I is regulated by N-acetylcysteine in lymphocytes of patients with systemic lupus erythematosusT cell activation-induced mitochondrial hyperpolarization is mediated by Ca2+- and redox-dependent production of nitric oxide.Different responses of astrocytes and neurons to nitric oxide: the role of glycolytically generated ATP in astrocyte protection.Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus.Inhibition of mitochondrial respiration by endogenous nitric oxide: a critical step in Fas signaling.Antitumor and angiostatic activities of the antimicrobial peptide dermaseptin B2.Mechanistic target of rapamycin activation triggers IL-4 production and necrotic death of double-negative T cells in patients with systemic lupus erythematosus.Mating-responsive genes in reproductive tissues of female Drosophila melanogaster.Activation of mammalian target of rapamycin controls the loss of TCRzeta in lupus T cells through HRES-1/Rab4-regulated lysosomal degradationOxidative stress, inflammation and carcinogenesis are controlled through the pentose phosphate pathway by transaldolaseThe role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosusViolacein induces cell death by triggering mitochondrial membrane hyperpolarization in vitro.Discovery of safe and orally effective 4-aminoquinaldine analogues as apoptotic inducers with activity against experimental visceral leishmaniasis.The effect of nitric oxide on cell respiration: A key to understanding its role in cell survival or death.Nitric oxide, mitochondrial hyperpolarization, and T cell activation.Sunlight inhibits growth and induces markers of programmed cell death in Plasmodium falciparum in vitro.Glutathione depletion is necessary for apoptosis in lymphoid cells independent of reactive oxygen species formationT cells expanded in presence of IL-15 exhibit increased antioxidant capacity and innate effector molecules.Reactive oxygen species and cellular oxygen sensingMetabolic control of T cell activation and death in SLE.
P2860
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P2860
Elevation of mitochondrial transmembrane potential and reactive oxygen intermediate levels are early events and occur independently from activation of caspases in Fas signaling
description
1999 nî lūn-bûn
@nan
1999 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@ast
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@en
type
label
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@ast
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@en
prefLabel
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@ast
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@en
P2093
P2860
P1476
Elevation of mitochondrial tra ...... n of caspases in Fas signaling
@en
P2093
P2860
P304
P407
P50
P577
1999-02-01T00:00:00Z