about
The sedoheptulose kinase CARKL directs macrophage polarization through control of glucose metabolismThe metabolic core and catalytic switches are fundamental elements in the self-regulation of the systemic metabolic structure of cellsTransaldolase is essential for maintenance of the mitochondrial transmembrane potential and fertility of spermatozoa.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.Mitochondrial hyperpolarization: a checkpoint of T-cell life, death and autoimmunity.T-cell and B-cell signaling biomarkers and treatment targets in lupus.T cell activation-induced mitochondrial hyperpolarization is mediated by Ca2+- and redox-dependent production of nitric oxide.Increased cellular proliferation and inflammatory cytokines in tonsils derived from children with obstructive sleep apneaZNF143 mediates basal and tissue-specific expression of human transaldolase.Time and Demand are Two Critical Dimensions of Immunometabolism: The Process of Macrophage Activation and the Pentose Phosphate Pathway.The UVB-Stimulated Expression of Transglutaminase 1 Is Mediated Predominantly via the NFκB Signaling Pathway: New Evidence of Its Significant Attenuation through the Specific Interruption of the p38/MSK1/NFκBp65 Ser276 Axis.Nitric oxide, mitochondrial hyperpolarization, and T cell activation.Programmed death-1 controls T cell survival by regulating oxidative metabolism.Glutathione depletion is necessary for apoptosis in lymphoid cells independent of reactive oxygen species formationCalcium signalling and cell-fate choice in B cells.Metabolic control of T cell activation and death in SLE.Antioxidant treatment reduces expansion and contraction of antigen-specific CD8+ T cells during primary but not secondary viral infection.Metabolic Factors that Contribute to Lupus PathogenesisActivation of the Mechanistic Target of Rapamycin in SLE: Explosion of Evidence in the Last Five Years.Immune Cell Metabolism in Systemic Lupus Erythematosus.Enhancement of mitochondrial ATP production by the Escherichia coli cytotoxic necrotizing factor 1.Mitochondrial complex I activity is impaired during HIV-1-induced T-cell apoptosis.Imaging in detecting sites of pulmonary fibrosis induced by paraquat.SLCO/OATP-like transport of glutathione in FasL-induced apoptosis: glutathione efflux is coupled to an organic anion exchange and is necessary for the progression of the execution phase of apoptosis.Astaxanthin attenuates the UVB-induced secretion of prostaglandin E2 and interleukin-8 in human keratinocytes by interrupting MSK1 phosphorylation in a ROS depletion-independent manner.Metabolic enhancers supporting 1-carbon cycle affect sperm functionality: an in vitro comparative study
P2860
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P2860
description
2002 nî lūn-bûn
@nan
2002 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Metabolic switches of T-cell activation and apoptosis.
@ast
Metabolic switches of T-cell activation and apoptosis.
@en
Metabolic switches of T-cell activation and apoptosis.
@nl
type
label
Metabolic switches of T-cell activation and apoptosis.
@ast
Metabolic switches of T-cell activation and apoptosis.
@en
Metabolic switches of T-cell activation and apoptosis.
@nl
prefLabel
Metabolic switches of T-cell activation and apoptosis.
@ast
Metabolic switches of T-cell activation and apoptosis.
@en
Metabolic switches of T-cell activation and apoptosis.
@nl
P2093
P1476
Metabolic switches of T-cell activation and apoptosis.
@en
P2093
Ferenc Puskas
Katalin Banki
Peter Gergely
P304
P356
10.1089/15230860260196227
P50
P577
2002-06-01T00:00:00Z