PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21833829-2 2012 It initializes the polyol pathway and under hyperglycemic conditions, catalyzes the conversion of glucose into sorbitol in the presence of NADPH. Glucose 98-105 2,4-dienoyl-CoA reductase 1 Homo sapiens 139-144 17636013-5 2007 Although DecR1 expression does not affect glucose uptake in ErbB2/Neu-transformed cells, sustained expression of DecR1 protects mammary tumor cells from apoptotic cell death following glucose withdrawal. Glucose 184-191 2,4-dienoyl-CoA reductase 1 Homo sapiens 113-118 34895333-11 2021 Furthermore, HK1 revertants but not HK2 revertants caused a strong increase of NADPH/NADP ratios independently on the presence of glucose or metformin. Glucose 130-137 2,4-dienoyl-CoA reductase 1 Homo sapiens 79-84 15983215-3 2005 In pancreatic beta-cells, glucose acutely raised the NADPH-to-NADP+ ratio and stimulated insulin release in parallel. Glucose 26-33 2,4-dienoyl-CoA reductase 1 Homo sapiens 53-58 12622692-8 2003 One of these factors is glucose, the metabolic products of which (ATP and NADPH) appear to participate in signalling pathways by supporting a precise onset of tyrosine phosphorylation in the sperm flagellum leading to successful fertilization. Glucose 24-31 2,4-dienoyl-CoA reductase 1 Homo sapiens 74-79 8052153-3 1994 The NADPH used by glutathione reductase for the reduction of oxidized glutathione (GSSG) to GSH is also used by aldose reductase for the reduction of glucose to sorbitol through the polyol pathway. Glucose 150-157 2,4-dienoyl-CoA reductase 1 Homo sapiens 4-9 34476741-10 2021 A high rate of aerobic glycolysis is induced by c-MYC, increasing the amounts of intracellular Glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), and glyceraldehyde-3-phosphate (GA3P), which can all enter pentose phosphate pathway (PPP) to produce Ribose-5-Phosphate (R5P) and NADPH, which are necessary for the biosynthesis of biomolecules such as proteins, nucleic acids, or lipids. Glucose 95-102 2,4-dienoyl-CoA reductase 1 Homo sapiens 281-286 33636336-7 2021 Importantly, this process could be effectively reversed and rescued by 2DG (a glucose analog capable of producing NADPH, a key antioxidant), A769662 (an allosteric AMPK activator), and N-acetyl cysteine (NAC) (a ROS scavenger), indicating the presence of a vicious circle between AMPK inactivation and ROS in LKB1-mutant NSCLC cells under glucose starvation. Glucose 78-85 2,4-dienoyl-CoA reductase 1 Homo sapiens 114-119 35421237-7 2022 Investigation of SS glucose metabolism revealed that ME1 null cells exhibit higher rates of glycolysis and higher flux of glucose into the pentose phosphate pathway (PPP), which is necessary to produce NADPH. Glucose 122-129 2,4-dienoyl-CoA reductase 1 Homo sapiens 202-207 1183000-3 1975 The rate of appearance of NADPH fluorescence at 460 nm (excitation wavelength, 340 nm) is monitored and related to the glucose concentration in plasma or serum. Glucose 119-126 2,4-dienoyl-CoA reductase 1 Homo sapiens 26-31 3519822-4 1986 We observed that: the effect of glucose on mononuclear cell cortisol metabolism was not influenced by insulin; NADPH and NADH enhanced cortisol metabolism by disrupted cells, irrespective of whether the homogenates were dialysed or not; lactate and ATP inhibited mononuclear cell cortisol metabolism and almost all the glucose used was converted to lactate. Glucose 319-326 2,4-dienoyl-CoA reductase 1 Homo sapiens 111-116 33636336-7 2021 Importantly, this process could be effectively reversed and rescued by 2DG (a glucose analog capable of producing NADPH, a key antioxidant), A769662 (an allosteric AMPK activator), and N-acetyl cysteine (NAC) (a ROS scavenger), indicating the presence of a vicious circle between AMPK inactivation and ROS in LKB1-mutant NSCLC cells under glucose starvation. Glucose 339-346 2,4-dienoyl-CoA reductase 1 Homo sapiens 114-119 33259599-9 2020 Extensive metabolomics analysis at steady state and upon incubation with stable isotope-labeled tracers (U-13C-glucose, 13C,15N-glutamine, and U-13C-fructose) demonstrated dramatic impairments in early glycolysis (hexose phosphate levels), hexosemonophosphate shunt (required for the generation of the NADPH), and the total adenylate pool, which could explain the dramatic cell dysfunction displayed by the patient"s neutrophils. Glucose 111-118 2,4-dienoyl-CoA reductase 1 Homo sapiens 302-307 32745767-5 2020 In addition, the hexokinase activity, glucose-6-phosphate dehydrogenase (G6PD) activity, NADPH level, NADPH/NADP+ ratio and mitochondrial activity were higher in the sperm treated with moderate glucose than in those not treated with glucose. Glucose 194-201 2,4-dienoyl-CoA reductase 1 Homo sapiens 89-94 32745767-5 2020 In addition, the hexokinase activity, glucose-6-phosphate dehydrogenase (G6PD) activity, NADPH level, NADPH/NADP+ ratio and mitochondrial activity were higher in the sperm treated with moderate glucose than in those not treated with glucose. Glucose 194-201 2,4-dienoyl-CoA reductase 1 Homo sapiens 102-107 32369187-5 2020 Using P450 BM3 together with glucose dehydrogenase for regeneration of NADPH, we compared soluble and co-immobilized enzymes in O2 -gassed and pH-controlled conversions at high final substrate concentrations (>= 40 mM). Glucose 29-36 2,4-dienoyl-CoA reductase 1 Homo sapiens 71-76 30571714-12 2018 Pathway analysis revealed that PMA affected nicotinate and nicotinamide metabolism, aminoacyl-tRNA biosynthesis and glycolysis, suggesting a redirection of glucose metabolism from glycolysis to the pentose phosphate pathway and production of NADPH for activation of the NADPH oxidase and subsequent respiratory burst. Glucose 156-163 2,4-dienoyl-CoA reductase 1 Homo sapiens 242-247 30571714-12 2018 Pathway analysis revealed that PMA affected nicotinate and nicotinamide metabolism, aminoacyl-tRNA biosynthesis and glycolysis, suggesting a redirection of glucose metabolism from glycolysis to the pentose phosphate pathway and production of NADPH for activation of the NADPH oxidase and subsequent respiratory burst. Glucose 156-163 2,4-dienoyl-CoA reductase 1 Homo sapiens 270-275 29125492-3 2017 Rather, compromise of glucose uptake facilitates glucose flux through glycolysis and may possibly decrease flux through the pentose phosphate pathway (PPP), limiting subsequent NADPH and GSH production needed for antioxidant protection. Glucose 22-29 2,4-dienoyl-CoA reductase 1 Homo sapiens 177-182 23702245-2 2013 Under physiological conditions glucose metabolism is linked to control of the NADH/NAD redox couple, as well as providing the major reductant, NADPH, for thiol-dependent antioxidant defenses. Glucose 31-38 2,4-dienoyl-CoA reductase 1 Homo sapiens 143-148 22926048-3 2013 HEDS is rapidly detoxified in normal glucose but triggered a p53-independent metabolic stress in glucose depleted state that caused loss of NADPH, protein and non-protein thiol homeostasis and Ku function, and enhanced sensitivity of both p53 wild type and mutant cells to radiation induced oxidative stress. Glucose 97-104 2,4-dienoyl-CoA reductase 1 Homo sapiens 140-145 32827651-5 2020 We show that glucose induces NADPH oxidase derived reactive oxygen species and further citrullinates the histones to form weaker NETs leading to reduced response to lipopolysaccharide (LPS). Glucose 13-20 2,4-dienoyl-CoA reductase 1 Homo sapiens 29-34 32827651-7 2020 NADPH is an absolute requirement for three independent pathways of formation of 1-anhydrosorbitol via aldose reductase under excess glucose, induction of glutathione synthesis and glucose induced NETs formation. Glucose 132-139 2,4-dienoyl-CoA reductase 1 Homo sapiens 0-5 32827651-7 2020 NADPH is an absolute requirement for three independent pathways of formation of 1-anhydrosorbitol via aldose reductase under excess glucose, induction of glutathione synthesis and glucose induced NETs formation. Glucose 180-187 2,4-dienoyl-CoA reductase 1 Homo sapiens 0-5 32827651-8 2020 During T2D and in presence of high glucose, there is a competition for NADPH between these processive reactions, which leads to its insufficiency to produce NETs in response to LPS. Glucose 35-42 2,4-dienoyl-CoA reductase 1 Homo sapiens 71-76 32273282-3 2020 Glucose starvation suppressed H2Aub levels independently of energy stress-mediated AMPK activation and possibly through NADPH depletion and subsequent inhibition of BMI1, an integral component of polycomb repressive complex 1 (PRC1) that catalyzes H2Aub on chromatin. Glucose 0-7 2,4-dienoyl-CoA reductase 1 Homo sapiens 120-125 32282309-5 2021 Furthermore, some molecules like HIF, PKM2, NADPH and others are essential to the survival of cancer cells into the hypoxic abnormal environment which has limited glucose sources. Glucose 163-170 2,4-dienoyl-CoA reductase 1 Homo sapiens 44-49 31557707-1 2019 The glucose metabolism in the pentose cycle is essential to the source of NADPH. Glucose 4-11 2,4-dienoyl-CoA reductase 1 Homo sapiens 74-79 26568303-0 2016 NAMPT suppresses glucose deprivation-induced oxidative stress by increasing NADPH levels in breast cancer. Glucose 17-24 2,4-dienoyl-CoA reductase 1 Homo sapiens 76-81 26568303-8 2016 Collectively, our results suggest a novel mechanism by which tumor cells protect themselves against glucose deprivation-induced oxidative stress by utilizing NAMPT to maintain NADPH levels. Glucose 100-107 2,4-dienoyl-CoA reductase 1 Homo sapiens 176-181