Πλοήγηση ανά Θέμα "Tryptophan"
Αποτελέσματα 1-10 από 10
-
Activation of general control nonderepressible 2 kinase protects human glomerular endothelial cells from harmful high-glucose-induced molecular pathways
(2016)Purpose: Considering the referred beneficial effects of protein restriction on diabetic nephropathy (DN) and the role of renal endothelium in its pathogenesis, we evaluated the effect of general control nonderepressible 2 ... -
Activation of general control nonderepressible-2 kinase ameliorates glucotoxicity in human peritoneal mesothelial cells, preserves their integrity, and prevents mesothelial to mesenchymal transition
(2019)Along with infections, ultrafiltration failure due to the toxicity of glucose-containing peritoneal dialysis (PD) solutions is the Achilles’ heel of PD method. Triggered by the protective effect of general control ... -
IDO decreases glycolysis and glutaminolysis by activating GCN2K, while it increases fatty acid oxidation by activating AhR, thus preserving CD4+ T-cell survival and proliferation
(2018)It is generally hypothesized in the literature that indoleamine 2,3-dioxygenase (IDO), by degrading L-tryptophan along the kynurenine pathway, suppresses CD4+ T-cell function by inducing apoptosis, inhibiting proliferation ... -
Indoleamine 2, 3-dioxygenase Up-regulates Hypoxia-inducible Factor-1α Expression by degrading l-Tryptophan but not its activity in human alloreactive t-cells
(2018)Indoleamine 2, 3-dioxygenase (IDO) suppresses T-cell function at least in part by altering cell metabolism. Hypoxia-inducible factor-1 (HIF-1) increases upon T-cell activation and alters cell metabolism favoring their ... -
Indoleamine 2,3-dioxygenase, by degrading L-tryptophan, enhances carnitine palmitoyltransferase i activity and fatty acid oxidation, and exerts fatty acid-dependent effects in human alloreactive CD4+ T-cells
(2016)Indoleamine 2,3-dioxygenase (IDO) is expressed in antigen presenting cells and by degrading L-tryptophan along the kynurenine pathway suppresses CD4+ T-cell proliferation, induces apoptosis and promotes differentiation ... -
Preconditioning of primary human renal proximal tubular epithelial cells without tryptophan increases survival under hypoxia by inducing autophagy
(2017)Purpose: Hypoxia plays a significant role in the pathogenesis of acute kidney injury (AKI). Autophagy protects from AKI. Amino acid deprivation induces autophagy. The effect of l-tryptophan depletion on survival and autophagy ... -
The role of indoleamine 2,3-dioxygenase in renal tubular epithelial cells senescence under anoxia or reoxygenation
(2021)Ischemia-reperfusion injury is the commonest form of acute kidney injury (AKI). Tubular epithelial cell senescence contributes to incomplete recovery from AKI and predisposes to subsequent chronic kidney disease. In cultures ... -
Tryptophan depletion under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through reactive oxygen species-dependent and independent pathways
(2017)In atherosclerosis-associated pathologic entities characterized by malnutrition and inflammation, l-tryptophan (TRP) levels are low. Insulin resistance is an independent cardiovascular risk factor and induces endothelial ... -
Tryptophan-kynurenine profile in pediatric autoimmune hepatitis
(2019)The impairment of regulatory T cells (Tregs) is a characteristic feature of autoimmune hepatitis (AIH), and the degradation of tryptophan (Trp) to kynurenine (Kyn), by gamma interferon-induced indoleamine-2,3-dioxygenase-1 ... -
What may constrain the success of indoleamine 2,3-dioxygenase 1 inhibitors in cancer immunotherapy?
(2018)[No abstract available]