PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33497360-2 2021 The pentose phosphate pathway (PPP), a metabolic pathway parallel to glycolysis, generates NADPH as a reducing equivalent and ribose 5-phosphate for nucleotide synthesis. Pentosephosphates 4-21 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 91-96 32853822-3 2020 Macrophages activation under FBW7 deficiency decreases substrate flux through the pentose phosphate pathway (PPP) to produce less equivalents (NADPH and GSH) and aggravate the generation of intracellular reactive oxygen species (ROS) in macrophages, thereby over-activating proinflammatory reaction. Pentosephosphates 82-99 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 143-148 33222382-3 2020 NADPH is produced principally by the housekeeping enzyme glucose-6-phosphate dehydrogenase (G6PD), which catalyzes the rate-limiting step in the pentose phosphate pathway. Pentosephosphates 145-162 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 0-5 33142766-3 2020 Indeed, previous studies reported a close link between FDG uptake and activation of a specific pentose phosphate pathway (PPP), triggered by hexose-6P-dehydrogenase (H6PD) and contributing to fuel NADPH-dependent antioxidant responses in the endoplasmic reticulum (ER). Pentosephosphates 95-112 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 197-202 24872551-1 2014 TP53-induced glycolysis and apoptosis regulator (TIGAR) inhibits glycolysis and increases the flow of pentose phosphate pathway (PPP), which generates NADPH and pentose. Pentosephosphates 102-119 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 151-156 31328803-4 2019 PKM2 inhibition increases substrate flux through the pentose phosphate pathway to generate reducing equivalents (NADPH and GSH) and protect against oxidative stress. Pentosephosphates 53-70 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 113-118 28473643-1 2017 Glucose-6-phosphate dehydrogenase (G6PD) is the first and rate-limiting enzyme of the pentose phosphate pathway; it catalyzes the conversion of glucose-6-phosphate to 6-phosphogluconate and NADP+ to NADPH and is thought to be the principal source of NADPH for the cytosolic glutathione and thioredoxin antioxidant defense systems. Pentosephosphates 86-103 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 199-204 28473643-1 2017 Glucose-6-phosphate dehydrogenase (G6PD) is the first and rate-limiting enzyme of the pentose phosphate pathway; it catalyzes the conversion of glucose-6-phosphate to 6-phosphogluconate and NADP+ to NADPH and is thought to be the principal source of NADPH for the cytosolic glutathione and thioredoxin antioxidant defense systems. Pentosephosphates 86-103 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 250-255 28852166-5 2017 Model simulations also reveal that pentose phosphate pathway and oxidative phosphorylation activities were kept at minimal levels to ensure NADPH production and anabolic precursors synthesis. Pentosephosphates 35-52 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 140-145 26710800-6 2016 In addition, pharmacologic inhibition of the pentose phosphate pathway decreased rates of disulfide reduction and proteolysis in the phagosome, implicating NADPH as a source of phagosomal reductive energy. Pentosephosphates 45-62 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 156-161 19822207-3 2010 Conflicting data exist regarding the effect of pO(2) on NADPH production via the oxidative pentose phosphate cycle (OPPC). Pentosephosphates 91-108 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 56-61 34662447-8 2022 Bioinformatic integration revealed a significant shunting of glucose away from glycolysis-citrate cycle and glycerol-lipid genesis to pentose phosphate cycle for NADPH/GSH/GSSG redox and pentose moieties for purine and pyrimidine nucleotides, and glycosylation/glucuronidation. Pentosephosphates 134-151 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 162-167 16213215-5 2005 We show that pentose-phosphate-pathway generation of NADPH is critical for oocyte survival and that the target of this regulation is caspase-2, previously shown to be required for oocyte death in mice. Pentosephosphates 13-30 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 53-58 15896329-1 2005 6-Phosphogluconate dehydrogenase (6PGDH) constitutes the pentose phosphate pathway and produces NADPH. Pentosephosphates 57-74 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 96-101 34522704-2 2021 Recent studies showed that, to prevent toxic buildup of highly insoluble cystine inside cells, cancer cells with high expression of SLC7A11 (SLC7A11high) are forced to quickly reduce cystine to more soluble cysteine, which requires substantial NADPH supply from the glucose-pentose phosphate pathway (PPP) route, thereby inducing glucose- and PPP-dependency in SLC7A11high cancer cells. Pentosephosphates 274-291 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 244-249 34845393-4 2021 Here we show using stable isotope tracing in mice that de novo lipogenesis in adipose is supported by glucose and its catabolism via the pentose phosphate pathway to make NADPH. Pentosephosphates 137-154 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 171-176 33964586-8 2021 Hyperglycosylation activated glucose-6-phosphate dehydrogenase (G6PDH), the rate-limiting enzyme in the pentose phosphate pathway, resulting in an upregulation of NADPH/NADP+ and GSH/GSSG couples and enhancement of redox homeostasis in the heart. Pentosephosphates 104-121 2,4-dienoyl CoA reductase 1, mitochondrial Mus musculus 163-168