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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)The three-dimensional structure of human transaldolaseCloning and expression of the human gene for transaldolase. A novel highly repetitive element constitutes an integral part of the coding sequence.Mitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosusThe pathogenesis of transaldolase deficiencyThe human transaldolase gene (TALDO1) is located on chromosome 11 at p15.4-p15.5Evaluation of autoimmunity to transaldolase in multiple sclerosisCCL genes in multiple sclerosis and systemic lupus erythematosusAdhesion-dependent Skp2 transcription requires selenocysteine tRNA gene transcription-activating factor (STAF)Transaldolase is essential for maintenance of the mitochondrial transmembrane potential and fertility of spermatozoa.Liver injury correlates with biomarkers of autoimmunity and disease activity and represents an organ system involvement in patients with systemic lupus erythematosus.Cleavage of transaldolase by granzyme B causes the loss of enzymatic activity with retention of antigenicity for multiple sclerosis patients.Elevation of mitochondrial transmembrane potential and reactive oxygen intermediate levels are early events and occur independently from activation of caspases in Fas signalingSystems 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.Attention deficit and hyperactivity disorder scores are elevated and respond to N-acetylcysteine treatment in patients with systemic lupus erythematosus.Metabolic control of the epigenome in systemic Lupus erythematosus.Tuberous sclerosis and fulminant lupus in a young woman.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.Infection in systemic lupus erythematosus: friend or foe?Pathogenic mechanisms in systemic lupus erythematosus.Emerging new pathways of pathogenesis and targets for treatment in systemic lupus erythematosus and Sjogren's syndrome.Oxidative stress in the pathology and treatment of systemic lupus erythematosusHRES-1/Rab4-mediated depletion of Drp1 impairs mitochondrial homeostasis and represents a target for treatment in SLE.T-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.Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus.Genetic and metabolic control of the mitochondrial transmembrane potential and reactive oxygen intermediate production in HIV disease.ZNF143 mediates basal and tissue-specific expression of human transaldolase.Mechanistic target of rapamycin activation triggers IL-4 production and necrotic death of double-negative T cells in patients with systemic lupus erythematosus.Oxidative Stress and ADHD: A Meta-Analysis.Mechanistic target of rapamycin complex 1 expands Th17 and IL-4+ CD4-CD8- double-negative T cells and contracts regulatory T cells in systemic lupus erythematosus.CD8+ T cell-mediated HLA-A*0201-restricted cytotoxicity to transaldolase peptide 168-176 in patients with multiple sclerosis.Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homoeostasis and apoptosis signal processing.Endothelial nitric oxide synthase reduces crescentic and necrotic glomerular lesions, reactive oxygen production, and MCP1 production in murine lupus nephritisMetabolic switches of T-cell activation and apoptosis.Activation of mammalian target of rapamycin controls the loss of TCRzeta in lupus T cells through HRES-1/Rab4-regulated lysosomal degradation
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hulumtues
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wetenschapper
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հետազոտող
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Andras Perl
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Andras Perl
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Andras Perl
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Andras Perl
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label
Andras Perl
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Andras Perl
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Andras Perl
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Andras Perl
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Andras Perl
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Andras Perl
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Andras Perl
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Andras Perl
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P106
P1153
7004626121
P21
P31
P496
0000-0002-5017-1348