PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 788424-1 1976 Somatostatin inhibits in a dose-dependent manner the glucagon secretion in the presence of up to 5 mM glucose, whereas the suppressed glucagon release in the presence of greater than or equal to 10 mM glucose, 10 mM glyceraldehyde, 30 mM fructose or 30 mM mannose is characterized by an increase of hormone release under the influence of somatostatin. Glyceraldehyde 216-230 somatostatin Rattus norvegicus 0-12 235531-7 1975 In the reduction of D-glyceraldehyde, catalyzed by aldehyde reductase, the pro-4R "A" hydrogen of NADPH attacks the re face of the carbonyl group. Glyceraldehyde 20-36 aldo-keto reductase family 1 member A1 Sus scrofa 51-69 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Glyceraldehyde 355-369 glycogen synthase kinase 3 beta Mus musculus 55-60 4288649-0 1966 A study of the reaction of glyceraldehyde with glyceraldehyde 3-phosphate dehydrogenase. Glyceraldehyde 27-41 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 47-87 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Glyceraldehyde 371-373 glycogen synthase kinase 3 beta Mus musculus 55-60 32992566-4 2020 We previously reported that GA-derived toxic advanced glycation end products (toxic AGEs, TAGE) induce AD-like alterations including intracellular tau phosphorylation. Glyceraldehyde 28-30 microtubule associated protein tau Homo sapiens 147-150 33536515-0 2021 RasGRP2 inhibits glyceraldehyde-derived toxic advanced glycation end-products from inducing permeability in vascular endothelial cells. Glyceraldehyde 17-31 RAS guanyl releasing protein 2 Homo sapiens 0-7 32208122-4 2021 METHOD: The assay of aldose reductase was performed by using NADPH as starting material and DL-Glyceraldehyde as a substrate. Glyceraldehyde 92-109 aldo-keto reductase family 1 member B Homo sapiens 21-37 32422542-5 2020 In our assay, the test compounds can target either ETGE or DLG binding site, therefore facilitating the exploration of diverse Keap1-Nrf2 inhibitors. Glyceraldehyde 59-62 kelch-like ECH-associated protein 1 Mus musculus 127-132 32660150-8 2020 Catalase activity did not decrease with the accumulation of TAGE, while mitochondrial membrane depolarization was enhanced in cells treated with GA. Glyceraldehyde 145-147 catalase Homo sapiens 0-8 32422542-5 2020 In our assay, the test compounds can target either ETGE or DLG binding site, therefore facilitating the exploration of diverse Keap1-Nrf2 inhibitors. Glyceraldehyde 59-62 nuclear factor, erythroid derived 2, like 2 Mus musculus 133-137 30836629-1 2019 Human triokinase/flavin mononucleotide (FMN) cyclase (hTKFC) catalyzes the adenosine triphosphate (ATP)-dependent phosphorylation of D-glyceraldehyde and dihydroxyacetone (DHA), and the cyclizing splitting of flavin adenine dinucleotide (FAD). Glyceraldehyde 133-149 triokinase and FMN cyclase Homo sapiens 54-59 31261040-11 2019 DP-2 was identified as 2-(2,4difluorobenzylamino)-2-oxoacetic acid which is novel DLG degradant and not reported earlier to the best of our knowledge. Glyceraldehyde 82-85 transcription factor Dp-2 Homo sapiens 0-4 31604989-5 2019 Our results from protein docking and spectrofluorimetric analyses clearly show that vitamin K1 is a potent inhibitor of ALR2 and this inhibition is primarily mediated by the blockage of DL-glyceraldehyde binding to ALR2. Glyceraldehyde 186-203 aldo-keto reductase family 1 member B Homo sapiens 120-124 31604989-5 2019 Our results from protein docking and spectrofluorimetric analyses clearly show that vitamin K1 is a potent inhibitor of ALR2 and this inhibition is primarily mediated by the blockage of DL-glyceraldehyde binding to ALR2. Glyceraldehyde 186-203 aldo-keto reductase family 1 member B Homo sapiens 215-219 31604989-7 2019 Another deduction that we can derive from the experiments performed with pure protein is that ALR2 has three levels of affinity, first for NADPH, second for vitamin K1 and third for the substrate DL-glyceraldehyde. Glyceraldehyde 196-213 aldo-keto reductase family 1 member B Homo sapiens 94-98 31002973-8 2019 The higher membrane damage, oxidative DNA damage and inflammation induced by AES1 in A549 cells could be due to the higher DLG and silica percentage. Glyceraldehyde 123-126 TLE family member 5, transcriptional modulator Homo sapiens 77-81 29316860-1 2018 Advanced glycation end products (AGEs) formed from glyceraldehyde (Gcer) and glycolaldehyde (Gcol) are involved in the pathogenesis of diabetic complications, via interactions with a receptor for AGEs (RAGE). Glyceraldehyde 51-65 advanced glycosylation end product-specific receptor Rattus norvegicus 202-206 29316860-1 2018 Advanced glycation end products (AGEs) formed from glyceraldehyde (Gcer) and glycolaldehyde (Gcol) are involved in the pathogenesis of diabetic complications, via interactions with a receptor for AGEs (RAGE). Glyceraldehyde 67-71 advanced glycosylation end product-specific receptor Rattus norvegicus 202-206 28425930-2 2017 Some (hyper)thermophilic Archaea contain an enzyme, called non-phosphorylating glyceraldehyde-3-phosphate dehydrogenase (GAPN), which catalyzes the direct oxidation of glyceraldehyde-3-phosphate to 3-phosphoglycerate omitting adenosine 5"-triphosphate (ATP) formation by substrate-level-phosphorylation via phosphoglycerate kinase. Glyceraldehyde 79-94 phosphoglycerate kinase Saccharomyces cerevisiae S288C 307-330 28683414-1 2017 In this paper we designed and investigated bioanode with alcohol dehydrogenase (ADH) catalysing oxidation of glycerol and glyceraldehyde. Glyceraldehyde 122-136 aldo-keto reductase family 1 member A1 Homo sapiens 57-78 28683414-1 2017 In this paper we designed and investigated bioanode with alcohol dehydrogenase (ADH) catalysing oxidation of glycerol and glyceraldehyde. Glyceraldehyde 122-136 aldo-keto reductase family 1 member A1 Homo sapiens 80-83 29079763-4 2017 Among intracellular GA-AGEs, caspase-3 has been identified as a GA-AGE-modified protein with abrogated protein function. Glyceraldehyde 20-22 caspase 3 Homo sapiens 29-38 29079763-5 2017 Furthermore, the activation of caspase-3 and induction of hepatocyte apoptosis by camptothecin, a DNA-damaging agent, was suppressed by a treatment with GA. Glyceraldehyde 153-155 caspase 3 Homo sapiens 31-40 29079763-6 2017 These results suggest the inhibitory effects of GA-AGE-modified caspase-3 on the induction of DNA-damage-induced apoptosis, which is associated with hepatocyte necrosis. Glyceraldehyde 48-50 caspase 3 Homo sapiens 64-73 29079763-7 2017 Therefore, the suppression of necrosis, the inflammatory form of cell death, by the accumulation of GA-AGEs and GA-AGE-modified caspase-3 may represent a novel therapeutic target for the pathogenesis of NASH. Glyceraldehyde 112-114 caspase 3 Homo sapiens 128-137 28785145-10 2017 The dose-dependent production of some high-molecular-weight (HMW) complexes of HSP90beta, HSP70, and HSP27 was observed following administration of GA. We considered HMW complexes to be dimers and trimers with GA-AGEs-mediated aggregation. Glyceraldehyde 148-150 heat shock protein 90 alpha family class B member 1 Homo sapiens 79-88 28785145-10 2017 The dose-dependent production of some high-molecular-weight (HMW) complexes of HSP90beta, HSP70, and HSP27 was observed following administration of GA. We considered HMW complexes to be dimers and trimers with GA-AGEs-mediated aggregation. Glyceraldehyde 148-150 heat shock protein family A (Hsp70) member 4 Homo sapiens 90-95 28785145-10 2017 The dose-dependent production of some high-molecular-weight (HMW) complexes of HSP90beta, HSP70, and HSP27 was observed following administration of GA. We considered HMW complexes to be dimers and trimers with GA-AGEs-mediated aggregation. Glyceraldehyde 148-150 heat shock protein family B (small) member 1 Homo sapiens 101-106 28632197-5 2017 The interaction between GA-AGEs and the receptor for AGEs (RAGE) alters intracellular signaling, gene expression, and the release of pro-inflammatory molecules and also elicits the production of reactive oxygen species by human hepatocytes and hepatic stellate cells, all of which may contribute to the pathological changes associated with chronic liver diseases. Glyceraldehyde 24-26 long intergenic non-protein coding RNA 914 Homo sapiens 59-63 26304702-1 2015 We have previously found that glyceraldehyde-derived advanced glycation end products (glycer-AGEs) elicit oxidative stress generation and evoke inflammatory and thrombotic reactions through their higher binding affinity to RAGE (receptor for AGEs), thereby playing a role in vascular complications in diabetes. Glyceraldehyde 30-44 advanced glycosylation end product-specific receptor Rattus norvegicus 223-227 28109289-0 2017 Plantamajoside from Plantago asiatica modulates human umbilical vein endothelial cell dysfunction by glyceraldehyde-induced AGEs via MAPK/NF-kappaB. Glyceraldehyde 101-115 nuclear factor kappa B subunit 1 Homo sapiens 138-147 27337067-4 2016 The analysis of the transgenic cell lines showed that tomato SlAKR4B has enzyme activities toward d-galacturonic acid as well as glyceraldehyde and glyoxal, suggesting that the SlAKR4B gene encodes a functional enzyme in tomato. Glyceraldehyde 129-143 aldo-keto reductase 4B Solanum lycopersicum 61-68 27337067-4 2016 The analysis of the transgenic cell lines showed that tomato SlAKR4B has enzyme activities toward d-galacturonic acid as well as glyceraldehyde and glyoxal, suggesting that the SlAKR4B gene encodes a functional enzyme in tomato. Glyceraldehyde 129-143 aldo-keto reductase 4B Solanum lycopersicum 177-184 26587989-3 2015 In a previous study, we demonstrated that glyceraldehyde-derived AGEs increase APP and Abeta via ROS. Glyceraldehyde 42-56 amyloid beta (A4) precursor protein Mus musculus 87-92 26410776-2 2015 In the current manuscript, effect of glycation in structural changes of human serum albumin (HSA) by the metabolites of glucose such as glyoxal, methylglyoxal and glyceraldehyde was studied using different spectroscopy techniques. Glyceraldehyde 163-177 albumin Homo sapiens 78-91 26410776-2 2015 In the current manuscript, effect of glycation in structural changes of human serum albumin (HSA) by the metabolites of glucose such as glyoxal, methylglyoxal and glyceraldehyde was studied using different spectroscopy techniques. Glyceraldehyde 163-177 albumin Homo sapiens 93-96 25944913-13 2015 Fourth, NAMPT inhibition led to increased glyceraldehyde and erythrose levels in the cell. Glyceraldehyde 42-56 nicotinamide phosphoribosyltransferase Homo sapiens 8-13 26304819-4 2015 GA induced the production of GA-derived advanced glycation end-products (GA-AGEs) and cell apoptosis, glycolytic inhibition, decreases in the medium concentrations of diagnostic markers of AD, such as amyloid beta 1-42 (Abeta42), and increases in tau phosphorylation. Glyceraldehyde 0-2 microtubule associated protein tau Homo sapiens 247-250 25582325-1 2015 BACKGROUND: We have previously shown that serum levels of glyceraldehyde-derived advanced glycation end products (Gly-AGEs) are elevated under oxidative stress and/or diabetic conditions and associated with insulin resistance, endothelial dysfunction and vascular inflammation in humans. Glyceraldehyde 58-72 insulin Homo sapiens 207-214 25451588-7 2015 It was determined that DHRS3 also participates in the metabolism of other endogenous compounds, such as androstenedione, estrone, and DL-glyceraldehyde, and in the biotransformation of xenobiotics (e.g., NNK and acetohexamide) in addition to all-trans-retinal. Glyceraldehyde 134-151 dehydrogenase/reductase 3 Homo sapiens 23-28 25684943-9 2015 Furthermore, in an experiment using glyceraldehyde, which is a precursor of Glycer-AGEs, hnRNPM was found to be more easily glycated than the other proteins. Glyceraldehyde 36-50 heterogeneous nuclear ribonucleoprotein M Homo sapiens 89-95 25684943-10 2015 CONCLUSION: The results suggest that glyceraldehyde-modified hnRNPM alters gene expression. Glyceraldehyde 37-51 heterogeneous nuclear ribonucleoprotein M Homo sapiens 61-67 25582325-10 2015 CONCLUSIONS: The present study suggests that GLAP might be a main glyceraldehyde-related AGE structure in Gly-AGEs that bound to RAGE and subsequently elicited ROS generation and inflammatory and thrombogenic reactions in HUVECs. Glyceraldehyde 66-80 long intergenic non-protein coding RNA 914 Homo sapiens 129-133 19857486-3 2010 In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. Glyceraldehyde 35-49 intercellular adhesion molecule 1 Homo sapiens 153-159 25400631-10 2014 After invasion, GBS has the ability to subvert innate immunity by mechanisms like glycerinaldehyde-3-phosphate-dehydrogenase-dependent induction of IL-10 and beta-protein binding to the inhibitory phagocyte receptors sialic acid binding immunoglobulin-like lectin 5 and 14. Glyceraldehyde 82-98 interleukin 10 Homo sapiens 148-153 25400631-10 2014 After invasion, GBS has the ability to subvert innate immunity by mechanisms like glycerinaldehyde-3-phosphate-dehydrogenase-dependent induction of IL-10 and beta-protein binding to the inhibitory phagocyte receptors sialic acid binding immunoglobulin-like lectin 5 and 14. Glyceraldehyde 82-98 sialic acid binding Ig like lectin 5 Homo sapiens 217-265 20638753-5 2012 To investigate a functional link between the disorders diabetes and AD, the effect of 2 AGEs, pentosidine and glyceraldehydes-derived pyridinium (GLAP), was studied on BACE1 expression both in vivo, in streptozotocin treated rats, and in vitro in differentiated neuroblastoma cells. Glyceraldehyde 110-125 beta-secretase 1 Rattus norvegicus 168-173 21995300-2 2011 D-Glyceraldehyde (DGA) is the triose fragment common to the substrates for XI and TIM. Glyceraldehyde 0-16 triosephosphate isomerase 1 Homo sapiens 82-85 21995300-2 2011 D-Glyceraldehyde (DGA) is the triose fragment common to the substrates for XI and TIM. Glyceraldehyde 18-21 triosephosphate isomerase 1 Homo sapiens 82-85 21276782-10 2011 However, lysates from COS-7 cells transfected with AKR1B15 showed a 4.8-fold (with p-nitrobenzaldehyde) and 3.3-fold (with dl-glyceraldehyde) increase in enzyme activity compared with untransfected COS-7 cells. Glyceraldehyde 123-140 aldo-keto reductase family 1 member B15 Homo sapiens 51-58 21470398-7 2011 High extracellular potassium and 10 mM tolbutamide abrogated the inhibition of insulin secretion by GA. Glyceraldehyde, dihydroxyacetone, methylpyruvate, GLP-1, and forskolin, an activator of adenylate cyclase, did not abrogate the inhibition. Glyceraldehyde 104-118 insulin Homo sapiens 79-86 20561512-0 2010 Hepatocyte or serum albumin protein carbonylation by oxidized fructose metabolites: Glyceraldehyde or glycolaldehyde as endogenous toxins? Glyceraldehyde 84-98 albumin Rattus norvegicus 14-27 20148428-7 2010 We demonstrated that this double mutant can use D-GA, glycolaldehyde and the L-isomer, L-GA, as acceptor substrates. Glyceraldehyde 48-52 glutaminase 2 Homo sapiens 87-91 26291727-7 2015 For aldose reductase back reaction, the substrate affinity of glycerol to aldose reductase was one order lower than that of glyceraldehyde in forward reaction. Glyceraldehyde 124-138 aldo-keto reductase family 1 member B1 Rattus norvegicus 4-20 25374323-6 2014 hAR inhibitory activity was determined by measuring the rate of decline in the absorbance of NAPH at 340 nm using 0.5 mM NADPH, 10 mM D,L-glyceraldehyde, and 3.6 mU/mL hAR in phosphate buffer solution (0.2 M, pH 6.2). Glyceraldehyde 134-152 lymphatic vessel endothelial hyaluronan receptor 1 Homo sapiens 0-3 23894676-4 2013 A key enzyme for this pathway is aldehyde dehydrogenase from Thermoplasma acidophilum, which catalyzes the highly substrate specific oxidation of d-glyceraldehyde to d-glycerate. Glyceraldehyde 146-162 Aldehyde dehydrogenase Escherichia coli 33-55 23288619-0 2013 Cell hypertrophy and MEK/ERK phosphorylation are regulated by glyceraldehyde-derived AGEs in cardiomyocyte H9c2 cells. Glyceraldehyde 62-76 Eph receptor B1 Rattus norvegicus 25-28 21707087-1 2011 The isomerization of glyceraldehyde to dihydroxy acetone catalyzed by the active site of Sn-beta zeolite is investigated using the B3LYP density functional and MP2 levels of theory. Glyceraldehyde 21-35 tryptase pseudogene 1 Homo sapiens 160-163 21376711-10 2011 Glyceraldehyde and glycolaldehyde were also detoxified by mitochondrial aldehyde dehydrogenase (ALDH2) as ALDH2 inhibitors increased their cytotoxicity. Glyceraldehyde 0-14 aldehyde dehydrogenase 2 family member Homo sapiens 96-101 21376711-10 2011 Glyceraldehyde and glycolaldehyde were also detoxified by mitochondrial aldehyde dehydrogenase (ALDH2) as ALDH2 inhibitors increased their cytotoxicity. Glyceraldehyde 0-14 aldehyde dehydrogenase 2 family member Homo sapiens 106-111 19834782-0 2010 An alpha-glucosidase inhibitor, acarbose treatment decreases serum levels of glyceraldehyde-derived advanced glycation end products (AGEs) in patients with type 2 diabetes. Glyceraldehyde 77-91 sucrase-isomaltase Homo sapiens 3-20 19955489-3 2010 Among various subtypes of AGEs, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) induce the expressions of intercellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon-gamma and tumor necrosis factor-alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells. Glyceraldehyde 32-46 intercellular adhesion molecule 1 Homo sapiens 132-165 19955489-3 2010 Among various subtypes of AGEs, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) induce the expressions of intercellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon-gamma and tumor necrosis factor-alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells. Glyceraldehyde 32-46 CD40 molecule Homo sapiens 183-187 19955489-3 2010 Among various subtypes of AGEs, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) induce the expressions of intercellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon-gamma and tumor necrosis factor-alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells. Glyceraldehyde 32-46 interferon gamma Homo sapiens 220-268 19857486-3 2010 In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. Glyceraldehyde 35-49 CD40 molecule Homo sapiens 164-168 19857486-3 2010 In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. Glyceraldehyde 35-49 interferon gamma Homo sapiens 204-226 19857486-3 2010 In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. Glyceraldehyde 35-49 tumor necrosis factor Homo sapiens 231-264 19368378-1 2009 Catalyst control dominates in the asymmetric hydrogenations of largely unfunctionalized trisubstituted alkenes formed from lactic acid and glyceraldehyde, affording syn- and anti-aldol products of the type shown above. Glyceraldehyde 139-153 synemin Homo sapiens 165-168 19718465-3 2009 Hyperglycaemia was mimicked in vitro by incubation of TAFI with glyceraldehyde and in vivo by hyperglycaemic clamping of healthy volunteers. Glyceraldehyde 64-78 carboxypeptidase B2 Homo sapiens 54-58 19718465-6 2009 Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential. Glyceraldehyde 89-103 carboxypeptidase B2 Homo sapiens 9-13 18325492-1 2008 AKR1B10 is an aldose reductase (AR) homologue overexpressed in liver cancer and various forms of that enzyme in carcinomas catalyze the reduction of anticancer drugs, potential cytostatic drug, and dl-glyceraldehyde but do not catalyze the reduction of glucose. Glyceraldehyde 198-215 aldo-keto reductase family 1 member B10 Homo sapiens 0-7 19028477-6 2009 Carbonyl groups in some anticancer drugs and dl-glyceraldehyde are converted by AKR1B10 to their corresponding alcohols. Glyceraldehyde 45-62 aldo-keto reductase family 1 member B10 Homo sapiens 80-87 19028477-9 2009 Similarly, kinetic parameters K(m) and k(cat) (NADPH, DL-glyceraldehyde) for the reduction of dl-glyceraldehyde by wild-type AKR1B10 are 2.2+/-0.2 mM and 0.71+/-0.05 sec(-1), respectively. Glyceraldehyde 54-71 aldo-keto reductase family 1 member B10 Homo sapiens 125-132 19028477-9 2009 Similarly, kinetic parameters K(m) and k(cat) (NADPH, DL-glyceraldehyde) for the reduction of dl-glyceraldehyde by wild-type AKR1B10 are 2.2+/-0.2 mM and 0.71+/-0.05 sec(-1), respectively. Glyceraldehyde 94-111 aldo-keto reductase family 1 member B10 Homo sapiens 125-132 19028477-10 2009 Mutation of residue 299 from Cys to Ser in AKR1B10 reduces the protein affinity for dl-glyceraldehyde and enhances AKR1B10"s catalytic activity but overall catalytic efficiency is reduced. Glyceraldehyde 84-101 aldo-keto reductase family 1 member B10 Homo sapiens 43-50 19028477-11 2009 For dl-glyceraldehyde reduction that is catalyzed by the Cys299Ser mutant AKR1B10, K(m) is 15.8+/-1.0mM and k(cat) (NADPH, DL-glyceraldehyde) is 2.8+/-0.2 sec(-1). Glyceraldehyde 4-21 aldo-keto reductase family 1 member B10 Homo sapiens 74-81 19028477-11 2009 For dl-glyceraldehyde reduction that is catalyzed by the Cys299Ser mutant AKR1B10, K(m) is 15.8+/-1.0mM and k(cat) (NADPH, DL-glyceraldehyde) is 2.8+/-0.2 sec(-1). Glyceraldehyde 123-140 aldo-keto reductase family 1 member B10 Homo sapiens 74-81 18987578-8 2008 JMC-2004 IC50 for ALR-2 was determined colorimetrically with D-glyceraldehyde as a substrate. Glyceraldehyde 61-77 lens aldose reductase pseudogene Bos taurus 18-23 18276838-4 2008 Expressed and purified from bacteria using affinity chromatography, the AKR1A1 protein with a single histidine (6x-His) tag exhibited the greatest activity using two test substrates: p-nitrobenzaldehyde (5.09 +/- 0.16 micromol/min/mg of purified protein) and DL-glyceraldehyde (1.24 +/- 0.17 micromol/min/mg). Glyceraldehyde 259-276 aldo-keto reductase family 1 member A1 Homo sapiens 72-78 18325492-1 2008 AKR1B10 is an aldose reductase (AR) homologue overexpressed in liver cancer and various forms of that enzyme in carcinomas catalyze the reduction of anticancer drugs, potential cytostatic drug, and dl-glyceraldehyde but do not catalyze the reduction of glucose. Glyceraldehyde 198-215 aldo-keto reductase family 1 member B Homo sapiens 14-30 18325492-1 2008 AKR1B10 is an aldose reductase (AR) homologue overexpressed in liver cancer and various forms of that enzyme in carcinomas catalyze the reduction of anticancer drugs, potential cytostatic drug, and dl-glyceraldehyde but do not catalyze the reduction of glucose. Glyceraldehyde 198-215 aldo-keto reductase family 1 member B Homo sapiens 32-34 18325492-2 2008 Kinetic parameters for wild-type and C299S mutant AKR1B10 indicate that substitution of serine for cysteine at position 299 reduces the affinity of this protein for dl-glyceraldehyde and enhances its catalytic activity. Glyceraldehyde 165-182 aldo-keto reductase family 1 member B10 Homo sapiens 50-57 18458846-5 2008 METHODS: An established human HSC line, LI90, was exposed to a glyceraldehyde-derived-AGE (glycer-AGE), and the phenotypical changes of the LI90 cells were investigated. Glyceraldehyde 63-77 fucosyltransferase 1 (H blood group) Homo sapiens 30-33 17462779-4 2007 Here, we report the identification of glyceraldehydes (Gcer)- and glycolaldehyde (Gcol)-derived AGE as RAGE ligands and their presence in vivo. Glyceraldehyde 38-53 long intergenic non-protein coding RNA 914 Homo sapiens 103-107 17462779-4 2007 Here, we report the identification of glyceraldehydes (Gcer)- and glycolaldehyde (Gcol)-derived AGE as RAGE ligands and their presence in vivo. Glyceraldehyde 55-59 long intergenic non-protein coding RNA 914 Homo sapiens 103-107 16425980-5 2005 Various types of immunochemically distinct AGEs, which were prepared in vitro by incubating bovine serum albumin with glucose, glyceraldehyde or glycolaldehyde, significantly decreased endothelial mRNA levels of PEDF Furthermore, H2O2 dose-dependently suppressed PEDF gene expression in ECs. Glyceraldehyde 127-141 serpin family F member 1 Homo sapiens 212-216 16916947-3 2006 This study first shows that glyceraldehyde can be used as GK-bypassing oxidative substrate and then examines whether the triose can metabolically activate beta-cells with low glucose responsiveness. Glyceraldehyde 28-42 glucokinase Homo sapiens 58-60 16916947-8 2006 It is concluded that glucose low-responsive beta-cells can be metabolically activated by the GK-bypassing glyceraldehyde, increasing their acute biosynthetic response to glucose but not their maximal glucose-inducible biosynthetic capacity, which is considered subject to chronic regulation. Glyceraldehyde 106-120 glucokinase Homo sapiens 93-95 15796891-3 2005 While no type of AGE we examined changed the permeability of endothelial sheets, glyceraldehyde-derived AGE induced VEGF expression most significantly in astrocytes. Glyceraldehyde 81-95 vascular endothelial growth factor A Homo sapiens 116-120 15796891-4 2005 The expression of glial cell line-derived neurotrophic factor (GDNF), which reduces the vascular permeability, was decreased in the astrocytes by treatment with glyceraldehyde-derived AGE. Glyceraldehyde 161-175 glial cell derived neurotrophic factor Homo sapiens 18-61 15796891-4 2005 The expression of glial cell line-derived neurotrophic factor (GDNF), which reduces the vascular permeability, was decreased in the astrocytes by treatment with glyceraldehyde-derived AGE. Glyceraldehyde 161-175 glial cell derived neurotrophic factor Homo sapiens 63-67 15796891-5 2005 These results indicate that glyceraldehyde-derived AGE is the biologically active substance for astrocytes by regulating the VEGF and GDNF expression, which is causally contributing to an increase in the permeability of the BBB. Glyceraldehyde 28-42 vascular endothelial growth factor A Homo sapiens 125-129 15796891-5 2005 These results indicate that glyceraldehyde-derived AGE is the biologically active substance for astrocytes by regulating the VEGF and GDNF expression, which is causally contributing to an increase in the permeability of the BBB. Glyceraldehyde 28-42 glial cell derived neurotrophic factor Homo sapiens 134-138 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). Glyceraldehyde 59-73 gastric inhibitory polypeptide Homo sapiens 126-129 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). Glyceraldehyde 59-73 gastric inhibitory polypeptide Homo sapiens 154-157 15796891-0 2005 Glyceraldehyde-derived advanced glycation end-products preferentially induce VEGF expression and reduce GDNF expression in human astrocytes. Glyceraldehyde 0-14 vascular endothelial growth factor A Homo sapiens 77-81 15796891-0 2005 Glyceraldehyde-derived advanced glycation end-products preferentially induce VEGF expression and reduce GDNF expression in human astrocytes. Glyceraldehyde 0-14 glial cell derived neurotrophic factor Homo sapiens 104-108 15221334-3 2004 We have found that AGE derived from glyceraldehyde (glycer-AGE) and glycolaldehyde (glycol-AGE) showed strong neurotoxicity for primary cultured rat cortical neurons in vitro. Glyceraldehyde 36-50 renin binding protein Rattus norvegicus 19-22 15221334-10 2004 In the central nervous system, glyceraldehyde is generated via the glycolytic pathway from glyceraldehyde-3-phosphate by glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Glyceraldehyde 31-45 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 163-168 15823718-10 2005 Moreover, we have recently found that glyceraldehyde-derived AGEs, one of the representative ligands for RAGE, exerted cytopathic effects on cultured neuronal cells and that neurotoxic effect of diabetic serum was completely blocked by neutralizing antibodies against glyceraldehydes-derived AGEs. Glyceraldehyde 38-52 advanced glycosylation end product-specific receptor Mus musculus 105-109 15823718-10 2005 Moreover, we have recently found that glyceraldehyde-derived AGEs, one of the representative ligands for RAGE, exerted cytopathic effects on cultured neuronal cells and that neurotoxic effect of diabetic serum was completely blocked by neutralizing antibodies against glyceraldehydes-derived AGEs. Glyceraldehyde 268-283 advanced glycosylation end product-specific receptor Mus musculus 105-109 15265860-3 2004 KDG aldolase (KDGA) then catalyzes the cleavage of KDG to D-glyceraldehyde and pyruvate. Glyceraldehyde 58-74 class I fructose-bisphosphate aldolase Saccharolobus solfataricus 4-12 15265860-6 2004 In turn, the aldolase exhibits a remarkable lack of stereoselectivity in the condensation reaction of pyruvate and D-glyceraldehyde, forming a mixture of KDG and KDGal. Glyceraldehyde 115-131 class I fructose-bisphosphate aldolase Saccharolobus solfataricus 13-21 15221334-3 2004 We have found that AGE derived from glyceraldehyde (glycer-AGE) and glycolaldehyde (glycol-AGE) showed strong neurotoxicity for primary cultured rat cortical neurons in vitro. Glyceraldehyde 36-50 renin binding protein Rattus norvegicus 59-62 15221334-3 2004 We have found that AGE derived from glyceraldehyde (glycer-AGE) and glycolaldehyde (glycol-AGE) showed strong neurotoxicity for primary cultured rat cortical neurons in vitro. Glyceraldehyde 36-50 renin binding protein Rattus norvegicus 59-62 14551196-6 2004 We find that disrupting alrA, the gene encoding aldehyde reductase, results in the loss of alrA mRNA and AlrA protein and a decrease in the ability of cell lysates to reduce both glyceraldehyde and glucose in an NADPH-coupled reaction. Glyceraldehyde 179-193 aldo-keto reductase family 1 member A1 Homo sapiens 48-66 15330583-4 2004 A proposed mechanism for LuxS is an aldose-ketose isomerization of S-ribosylhomocysteine followed by a beta-elimination. Glyceraldehyde 36-42 Lutheran suppressor, X-linked Homo sapiens 25-29 14675555-5 2004 If glucose metabolism through the glycolytic pathway is impaired, as in insulin resistance, there will be a build-up of glyceraldehyde, glyceraldehyde-3-phosphate and dihydroxyacetone phosphate with further metabolism to methylglyoxal, a highly reactive ketoaldehyde. Glyceraldehyde 120-134 insulin Homo sapiens 72-79 12943535-8 2003 In addition, ALDH3A1 metabolized glyceraldehyde poorly and did not metabolize glucose 6-phosphate, 6-phosphoglucono-delta-lactone and 6-phosphogluconate at all, suggesting that this enzyme is not involved in either glycolysis or the pentose phosphate pathway. Glyceraldehyde 33-47 aldehyde dehydrogenase 3 family member A1 Homo sapiens 13-20 15019601-4 2004 Experiments with monocyte-enriched cultures revealed that RAGE mRNA and protein levels were down-regulated by the exposure to glyceraldehyde-derived AGE-the recently identified high-affinity RAGE ligand. Glyceraldehyde 126-140 advanced glycosylation end-product specific receptor Homo sapiens 58-62 15019601-4 2004 Experiments with monocyte-enriched cultures revealed that RAGE mRNA and protein levels were down-regulated by the exposure to glyceraldehyde-derived AGE-the recently identified high-affinity RAGE ligand. Glyceraldehyde 126-140 advanced glycosylation end-product specific receptor Homo sapiens 191-195 12633766-3 2003 Results Using D-BUT-CHT-lys-pNA as a plasmin-specific substrate, we show that incubation of plasma with fructose, glyceraldehyde or MG but not glucose decreases plasminogen activity reaching more than 40% in 16 h. A parallel dose-dependent decrease in heparin activation of AT III by up to a 50% was demonstrated using SAR-PRO-ARG-pNA as a specific thrombin substrate. Glyceraldehyde 114-128 serpin family C member 1 Homo sapiens 274-280 14599218-3 2003 The deoxypropionate subunit consisting of four alternating C-methyl groups with a C(4)-C(10) syn/syn/anti orientation was elaborated by a new method of iterative cuprate additions to acyclic alpha,beta-unsaturated esters relying on two consecutive 1,3-inductions and starting with d-glyceraldehyde as the chiral progenitor. Glyceraldehyde 281-297 synemin Homo sapiens 93-96 14577607-6 2003 These data suggest that the carbohydrates or glyceraldehyde were metabolised to form carbonyls such as MG which depleted erythrocyte GSH as a result of catalysis by glyoxalase I. Glyceraldehyde 45-59 glyoxalase I Homo sapiens 165-177 14599218-3 2003 The deoxypropionate subunit consisting of four alternating C-methyl groups with a C(4)-C(10) syn/syn/anti orientation was elaborated by a new method of iterative cuprate additions to acyclic alpha,beta-unsaturated esters relying on two consecutive 1,3-inductions and starting with d-glyceraldehyde as the chiral progenitor. Glyceraldehyde 281-297 synemin Homo sapiens 97-100 12633766-3 2003 Results Using D-BUT-CHT-lys-pNA as a plasmin-specific substrate, we show that incubation of plasma with fructose, glyceraldehyde or MG but not glucose decreases plasminogen activity reaching more than 40% in 16 h. A parallel dose-dependent decrease in heparin activation of AT III by up to a 50% was demonstrated using SAR-PRO-ARG-pNA as a specific thrombin substrate. Glyceraldehyde 114-128 coagulation factor II, thrombin Homo sapiens 349-357 11485558-1 2001 Modification of aldose reductase (AR) by the nitrosothiols S-nitroso-N-acetyl penicillamine (SNAP) and N-(beta-glucopyranosyl)-N(2)-acetyl-S-nitrosopenicillamide (glyco-SNAP) resulted in a 3-7-fold increase in its k(cat) and a 25-40-fold increase in its K(m) for glyceraldehyde. Glyceraldehyde 263-277 aldo-keto reductase family 1 member B Homo sapiens 16-32 12210903-8 2002 In comparison to other mammalian and yeast aldo-keto reductases, Ypr1p has relatively high affinity for D,L-glyceraldehyde (1.08 mM) and hexanal (0.39 mM), but relatively low affinity for 4-nitrobenzaldehyde (1.07 mM). Glyceraldehyde 104-122 trifunctional aldehyde reductase/carbonyl reductase (NADPH)/glucose 1-dehydrogenase (NADP(+)) YPR1 Saccharomyces cerevisiae S288C 65-70 12125098-3 2002 Almost complete inactivation of glyceraldehyde-3-phosphate dehydrogenase by treatment of cells with iodoacetate resulted in a 95% decrease in L-lactate formation from the ketotriose as well as from glucose, whereas L-lactate formation from the aldotriose was only partially reduced (60%). Glyceraldehyde 244-254 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 32-72 12135102-5 2002 Tectoridin and tectorigenin, exhibited the highest aldose reductase inhibitory potency, their IC50 values, being 1.08 x 10(-6) M and 1.12 x 10(-6) M, respectively, for DL-glyceraldehyde as a substrate. Glyceraldehyde 168-185 aldo-keto reductase family 1 member B1 Rattus norvegicus 51-67 12002523-5 2002 Glycating agents, methylglyoxal (MG) and glyceraldehyde (Glyc), caused an increase in the formation of advanced glycation endproducts (AGEs) in native and denatured GAPDH and AAT. Glyceraldehyde 41-55 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 165-170 12002523-5 2002 Glycating agents, methylglyoxal (MG) and glyceraldehyde (Glyc), caused an increase in the formation of advanced glycation endproducts (AGEs) in native and denatured GAPDH and AAT. Glyceraldehyde 0-4 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 165-170 11580274-4 2001 Both Cys-ALR2 and CysGly-ALR2 essentially retain the ability to reduce glyceraldehyde but lose the susceptibility to inhibition by Sorbinil and other ALR2 inhibitors. Glyceraldehyde 71-85 lens aldose reductase pseudogene Bos taurus 9-13 11580274-4 2001 Both Cys-ALR2 and CysGly-ALR2 essentially retain the ability to reduce glyceraldehyde but lose the susceptibility to inhibition by Sorbinil and other ALR2 inhibitors. Glyceraldehyde 71-85 lens aldose reductase pseudogene Bos taurus 25-29 11580274-4 2001 Both Cys-ALR2 and CysGly-ALR2 essentially retain the ability to reduce glyceraldehyde but lose the susceptibility to inhibition by Sorbinil and other ALR2 inhibitors. Glyceraldehyde 71-85 lens aldose reductase pseudogene Bos taurus 25-29 11958479-7 2002 Molecular modeling studies indicate that the energy-minimized structure of 3,4-dihydroxymandelaldehyde bound to aldose reductase is similar to that of glyceraldehyde where the 2"-hydroxyl group forms hydrogen bonds with Trp111 and NADPH. Glyceraldehyde 151-165 aldo-keto reductase family 1 member B Homo sapiens 112-128 11377826-5 2001 In paired experiments, stimulation of inositol phosphate (IP) accumulation by the fuel glyceraldehyde was enhanced in clones overexpressing PLC beta 1, in parallel with the G-protein alpha subunit activator, AlF(4)(-), suggesting a coupling between glyceraldehyde and this PLC isoform. Glyceraldehyde 87-101 phospholipase C beta 1 Rattus norvegicus 140-150 11377826-5 2001 In paired experiments, stimulation of inositol phosphate (IP) accumulation by the fuel glyceraldehyde was enhanced in clones overexpressing PLC beta 1, in parallel with the G-protein alpha subunit activator, AlF(4)(-), suggesting a coupling between glyceraldehyde and this PLC isoform. Glyceraldehyde 249-263 phospholipase C beta 1 Rattus norvegicus 140-150 11377826-9 2001 These studies illustrate unique pathways coupling diverse secretagogues to specific PLC isoforms in islet beta cells, and demonstrate that glyceraldehyde can activate PLC beta 1 but not PLC delta 1; whereas, vasopressin, but not carbachol, can stimulate either isoform. Glyceraldehyde 139-153 phospholipase C beta 1 Rattus norvegicus 167-177 11040087-0 2000 Aldose reductase does catalyse the reduction of glyceraldehyde through a stoichiometric oxidation of NADPH. Glyceraldehyde 48-62 aldose reductase Bos taurus 0-16 11040087-1 2000 In order to define the ability of bovine lens aldose reductase (ALR2) to generate polyols from aldoses, the quantitative determination of glycerol in the presence of glyceraldehyde was performed by gas chromatography after derivatization with trifluoroacetic anhydride. Glyceraldehyde 166-180 aldose reductase Bos taurus 46-62 11040087-1 2000 In order to define the ability of bovine lens aldose reductase (ALR2) to generate polyols from aldoses, the quantitative determination of glycerol in the presence of glyceraldehyde was performed by gas chromatography after derivatization with trifluoroacetic anhydride. Glyceraldehyde 166-180 lens aldose reductase pseudogene Bos taurus 64-68 10584067-3 1999 In this paper a computer simulation study is presented that utilizes the hybrid quantum mechanical and molecular mechanical (QM-MM) potential to elucidate the nature of the hydride and proton transfer steps in the reduction of D-glyceraldehyde by ALR2. Glyceraldehyde 227-243 aldo-keto reductase family 1 member B Homo sapiens 247-251 10926895-6 2000 RESULTS: The racemic mixture of glyceraldehyde (D,L-GA) preserved glucose concentrations for up to 8 h at room temperature. Glyceraldehyde 32-46 glutaminase 2 Homo sapiens 50-54 10926895-11 2000 CONCLUSIONS: Glyceraldehyde (D,L-GA or L-GA) effectively preserves glucose concentrations in whole blood specimens for up to 8 h. Specimens collected with D,L-GA or L-GA are suitable for analysis of many analytes commonly comeasured with glucose. Glyceraldehyde 13-27 glutaminase 2 Homo sapiens 31-35 10926895-11 2000 CONCLUSIONS: Glyceraldehyde (D,L-GA or L-GA) effectively preserves glucose concentrations in whole blood specimens for up to 8 h. Specimens collected with D,L-GA or L-GA are suitable for analysis of many analytes commonly comeasured with glucose. Glyceraldehyde 13-27 glutaminase 2 Homo sapiens 39-43 10926895-11 2000 CONCLUSIONS: Glyceraldehyde (D,L-GA or L-GA) effectively preserves glucose concentrations in whole blood specimens for up to 8 h. Specimens collected with D,L-GA or L-GA are suitable for analysis of many analytes commonly comeasured with glucose. Glyceraldehyde 13-27 glutaminase 2 Homo sapiens 39-43 10926895-11 2000 CONCLUSIONS: Glyceraldehyde (D,L-GA or L-GA) effectively preserves glucose concentrations in whole blood specimens for up to 8 h. Specimens collected with D,L-GA or L-GA are suitable for analysis of many analytes commonly comeasured with glucose. Glyceraldehyde 13-27 glutaminase 2 Homo sapiens 39-43 10629088-4 2000 The prooxidants hydrogen peroxide, menadione and glyceraldehyde raised ROS in large tumor spheroids and significantly down-regulated Pgp within 24 hr. Glyceraldehyde 49-63 ATP binding cassette subfamily B member 1 Homo sapiens 133-136 9733737-2 1998 In mice lacking the HNF-1alpha gene, insulin secretion and intracellular calcium ([Ca2+]i) responses were impaired following stimulation with nutrient secretagogues such as glucose and glyceraldehyde but normal with non-nutrient stimuli such as potassium chloride. Glyceraldehyde 185-199 HNF1 homeobox A Mus musculus 20-30 9633649-4 1998 The apparent K(m)s for the glycerol dehydrogenase was 16-fold higher for the glycerol than that for the glyceraldehyde in the case of the glyceraldehyde-3-phosphate dehydrogenase and fourfold higher for the NAD+, providing an explanation for the shift of the glycerol flow toward 1,3-propanediol when cells were grown on glucose-glycerol mixtures. Glyceraldehyde 104-118 gldA Clostridium butyricum 27-49 9972287-2 1998 Glucose, mannose, fructose, glyceraldehyde and dihydroxyacetone all at 8 mM, significantly enhanced the release of insulin elicited by basal concentrations of these carbohydrates (2 mM). Glyceraldehyde 28-42 insulin Homo sapiens 115-122 9546197-1 1998 The catalytic reduction of D-glyceraldehyde to glycerol by aldose reductase has been investigated with the combined potentials of quantum mechanics (QM) and molecular mechanics (MM) to resolve the question of whether Tyr48 or His110 serves as the proton donor during catalysis. Glyceraldehyde 27-43 aldo-keto reductase family 1 member B Homo sapiens 59-75 9546197-3 1998 Utilizing the combined potentials of QM and MM, the binding mode of substrate D-glyceraldehyde was investigated by optimizing the local geometry of Asp43, Lys77, Tyr48, His110 and NADPH at the active site of aldose reductase. Glyceraldehyde 78-94 aldo-keto reductase family 1 member B Homo sapiens 208-224 9224548-3 1997 Two K(+)-ATP channel openers (diazoxide and BPDZ44) inhibited; while a K(+)-ATP channel blocker (tolbutamide) and metabolizable sugars (glucose, glyceraldehyde) significantly stimulated the output of insulin. Glyceraldehyde 145-159 insulin Homo sapiens 200-207 9438984-1 1997 Human Cu,Zn-superoxide dismutase (SOD) was incubated with various intermediates of the Maillard reaction and glycolytic pathway (arabinose, glyoxal, glycolaldehyde, glyceraldehyde, glyceraldehyde 3-phosphate, and dihydroxyacetone) and some reducing sugars (sorbose, xylose, and ribose). Glyceraldehyde 165-179 superoxide dismutase 1 Homo sapiens 6-32 9438984-1 1997 Human Cu,Zn-superoxide dismutase (SOD) was incubated with various intermediates of the Maillard reaction and glycolytic pathway (arabinose, glyoxal, glycolaldehyde, glyceraldehyde, glyceraldehyde 3-phosphate, and dihydroxyacetone) and some reducing sugars (sorbose, xylose, and ribose). Glyceraldehyde 165-179 superoxide dismutase 1 Homo sapiens 34-37 9488002-2 1997 Treatment of RINm5F cells for 24 h with interleukin-1 beta (IL-1 beta) (100 pM) induced expression of nitric oxide synthase and inhibited glyceraldehyde-stimulated insulin secretion. Glyceraldehyde 138-152 interleukin 1 beta Rattus norvegicus 40-58 9488002-2 1997 Treatment of RINm5F cells for 24 h with interleukin-1 beta (IL-1 beta) (100 pM) induced expression of nitric oxide synthase and inhibited glyceraldehyde-stimulated insulin secretion. Glyceraldehyde 138-152 interleukin 1 beta Rattus norvegicus 60-69 9099732-11 1997 We conclude that RINm5F cells show steroid-sensitive plasticity and express NPY after dexamethasone treatment concomitantly with a decreased insulin secretion and impaired increase in cytosolic Ca2+ upon depolarization with KCl or stimulation with D-glyceraldehyde. Glyceraldehyde 248-264 neuropeptide Y Rattus norvegicus 76-79 9070901-2 1997 Islets from normal guinea pigs released insulin in a K+ and D-glyceraldehyde dependent manner showing a rapid initial secretion phase followed by secondary waves of insulin release during a 120 min period. Glyceraldehyde 60-76 insulin Cavia porcellus 40-47 9070901-2 1997 Islets from normal guinea pigs released insulin in a K+ and D-glyceraldehyde dependent manner showing a rapid initial secretion phase followed by secondary waves of insulin release during a 120 min period. Glyceraldehyde 60-76 insulin Cavia porcellus 165-172 9070901-4 1997 In contrast, insulin release from ascorbic acid deficient islets in response to the secretagogue, D-glyceraldehyde, was significantly delayed and decreased responses were observed during the 120 min period after D-glyceraldehyde stimulation. Glyceraldehyde 98-114 insulin Cavia porcellus 13-20 9070901-4 1997 In contrast, insulin release from ascorbic acid deficient islets in response to the secretagogue, D-glyceraldehyde, was significantly delayed and decreased responses were observed during the 120 min period after D-glyceraldehyde stimulation. Glyceraldehyde 212-228 insulin Cavia porcellus 13-20 9003425-3 1997 In cultures, sorbitol, commercial mannitol, fructose, D-glyceraldehyde or high concentrations of glucose caused fructose 1-phosphate formation and glucokinase translocation in parallel. Glyceraldehyde 54-70 glucokinase Rattus norvegicus 147-158 9074947-2 1997 Lineweaver-Burk plots revealed non-competitive inhibition between DL-glyceraldehyde or beta-NADPH and inhibition of AR by GP-1447. Glyceraldehyde 66-83 aldo-keto reductase family 1 member B1 Rattus norvegicus 116-118 8968865-3 1996 BACKGROUND: Somatostatin secretion from the endocrine pancreas is stimulated by glucose, glyceraldehyde, and dihydroxyacetone but not affected by fructose, galactose, or ribose. Glyceraldehyde 89-103 somatostatin Canis lupus familiaris 12-24 7657661-9 1995 Glycation with DL-glyceraldehyde showed an important role for both Gly-1 and Lys-2 in the glycation-mediated gamma B-crystallin cross-linking. Glyceraldehyde 15-32 crystallin gamma B Bos taurus 109-127 8920636-8 1996 This novel enzyme utilizes NADPH to reduce DL-glyceraldehyde and is clearly distinct from the other aldo-keto reductases in molecular weight, substrate specificity, inhibition by aldose reductase inhibitors and immunological properties. Glyceraldehyde 43-60 aldo-keto reductase family 1 member B1 Canis lupus familiaris 179-195 7558425-7 1995 The viability of hepatoma cells in the presence of 3-deoxyglucosone and glyceraldehyde was decreased by an aldose reductase inhibitor, ONO-2235 (5-[1Z,2E)-2-methyl-3-phenylpropenylidene]-4-oxo-2-thioxo -3- thiazolidineacetic acid). Glyceraldehyde 72-86 aldo-keto reductase family 1 member B1 Rattus norvegicus 107-123 8526867-5 1995 Determination of the apparent Km reveals that AFAR has highest affinity for 9,10-phenanthrenequinone and succinic semialdehyde, and low affinity for glyoxal and DL-glyceraldehyde. Glyceraldehyde 161-178 aldo-keto reductase family 7 member A3 Rattus norvegicus 46-50 7641310-2 1995 The apparent type of inhibition of rat lens aldose reductase by perillosides A and C was competitive with respect to glyceraldehyde and their K(i) values were 1.4 x 10(-4) and 2.3 x 10(-4) M, respectively. Glyceraldehyde 117-131 aldo-keto reductase family 1 member B1 Rattus norvegicus 44-60 7646447-0 1995 The stimulation of insulin secretion by D-glyceraldehyde correlates with its rate of oxidation in islet cells. Glyceraldehyde 40-56 insulin Homo sapiens 19-26 7646447-1 1995 D-Glyceraldehyde"s capacity to mimic the effect of D-glucose on insulin secretion has not yet been sufficiently substantiated. Glyceraldehyde 0-16 insulin Homo sapiens 64-71 7646447-7 1995 The ratio of the maximum insulin responses D-glyceraldehyde and D-glucose (57%) correlated with the ratio of their respective maximum rates of oxidation (68%). Glyceraldehyde 43-59 insulin Homo sapiens 25-32 7646447-10 1995 The lower potency of D-glyceraldehyde as an insulin secretagogue than D-glucose is determined by the lower capacity of islets to oxidize the triose compared with the hexose. Glyceraldehyde 21-37 insulin Homo sapiens 44-51 7831203-10 1994 These results indicate that porcine kidney triokinase has properties advantageous for the glyceraldehyde assay using glyceraldehyde-3-phosphate dehydrogenase as a coupling enzyme. Glyceraldehyde 90-104 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 117-157 7641075-3 1995 However, typical substrates for ALR such as D,L-glyceraldehyde, D-erythrose, D-glucuronate and p-carboxybenzaldehyde could not protect the enzyme from inactivation. Glyceraldehyde 44-62 aldo-keto reductase family 1 member B1 Bos taurus 32-35 7555597-2 1995 In the present study, the effects of non-enzymatic glycation of recombinant human AR (rhAR) on enzyme activity and affinity for its substrate (glyceraldehyde), co-factor (NADPH) and inhibitors (ARI; Sorbinil, Tolrestat, AL-1576 and Statil) were examined. Glyceraldehyde 143-157 aldo-keto reductase family 1 member B Homo sapiens 82-84 8028228-3 1994 SPR-210 showed a noncompetitive mechanism with respect to DL-glyceraldehyde against porcine lens AR. Glyceraldehyde 58-75 TGFB1-induced anti-apoptotic factor 1 Homo sapiens 0-7 8027987-4 1994 Compounds within these series were evaluated in vitro for their ability to inhibit glyceraldehyde reduction by bovine lens aldose reductase and in vivo by their ability to inhibit galactitol accumulation in the lens and sciatic nerve of galactose-fed rats. Glyceraldehyde 83-97 aldose reductase Bos taurus 123-139 8194074-4 1994 Isotopic tracer studies clearly show that the glyceraldehyde is produced by loss of C-1 from the starting L-threose molecule. Glyceraldehyde 46-60 heterogeneous nuclear ribonucleoprotein C Homo sapiens 84-87 8028228-3 1994 SPR-210 showed a noncompetitive mechanism with respect to DL-glyceraldehyde against porcine lens AR. Glyceraldehyde 58-75 aldo-keto reductase family 1 member B1 Rattus norvegicus 97-99 8504883-9 1993 Although the phospholipase A2 activator, melittin, initiated insulin release in the presence of 2 mM glucose and enhanced 10 mM glyceraldehyde-stimulated insulin secretion it had no effect on 20 mM glucose-induced insulin release. Glyceraldehyde 128-142 phospholipase A2 group IB Rattus norvegicus 13-29 8407226-6 1993 RESULTS: Throughout the purification steps, dehydrogenase activity with naphthalene dihydrodiol as substrate coeluted with aldose reductase activity assayed with DL-glyceraldehyde as substrate. Glyceraldehyde 162-179 aldo-keto reductase family 1 member B1 Rattus norvegicus 123-139 8343525-1 1993 Modification of human placental aldose reductase by iodoacetate (IAA) led to a mol/mol binding of IAA, a 40% decrease in the kcat, a 3-5-fold increase in the Km,NADPH and Km,glyceraldehyde and a 600-fold increase in the Ki,sorbinil; determined at pH 6.0. Glyceraldehyde 174-188 aldo-keto reductase family 1 member B Homo sapiens 32-48 8513967-0 1993 Inhibition of glucose-induced insulin secretion through inactivation of glucokinase by glyceraldehyde. Glyceraldehyde 87-101 glucokinase Rattus norvegicus 72-83 8513967-1 1993 D-Glyceraldehyde irreversibly inhibited rat liver glucokinase in a concentration-dependent manner. Glyceraldehyde 0-16 glucokinase Rattus norvegicus 50-61 8513967-2 1993 The inactivation of glucokinase by glyceraldehyde was blocked by the presence of its substrates such as glucose and mannose. Glyceraldehyde 35-49 glucokinase Rattus norvegicus 20-31 8513967-3 1993 Glucokinase was highly sensitive to glyceraldehyde compared with some other glycolytic enzymes (from animal tissues) including hexokinase, glucose-6-phosphate isomerase, 6-phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase. Glyceraldehyde 36-50 glucokinase Rattus norvegicus 0-11 8513967-4 1993 The amino acid analysis of untreated and glyceraldehyde-treated glucokinase suggested that glyceraldehyde-induced inactivation of glucokinase is caused by glycation of Lys residues of the enzyme by the triose. Glyceraldehyde 41-55 glucokinase Rattus norvegicus 64-75 8513967-4 1993 The amino acid analysis of untreated and glyceraldehyde-treated glucokinase suggested that glyceraldehyde-induced inactivation of glucokinase is caused by glycation of Lys residues of the enzyme by the triose. Glyceraldehyde 41-55 glucokinase Rattus norvegicus 130-141 8513967-4 1993 The amino acid analysis of untreated and glyceraldehyde-treated glucokinase suggested that glyceraldehyde-induced inactivation of glucokinase is caused by glycation of Lys residues of the enzyme by the triose. Glyceraldehyde 91-105 glucokinase Rattus norvegicus 64-75 8513967-4 1993 The amino acid analysis of untreated and glyceraldehyde-treated glucokinase suggested that glyceraldehyde-induced inactivation of glucokinase is caused by glycation of Lys residues of the enzyme by the triose. Glyceraldehyde 91-105 glucokinase Rattus norvegicus 130-141 8513967-5 1993 Treatment of pancreatic islets with 6 mM glyceraldehyde for 1 h at 37 degrees C caused both inactivation of glucokinase and inhibition of glucose-induced insulin secretion. Glyceraldehyde 41-55 glucokinase Rattus norvegicus 108-119 8513967-8 1993 When pancreatic islets were cultured with a lower concentration (1 mM) of glyceraldehyde for a longer time (17 h) in the presence of 10 mM glucose to mimic the in vivo conditions, both glucokinase activity and glucose-induced insulin secretion were again decreased. Glyceraldehyde 74-88 glucokinase Rattus norvegicus 185-196 8513967-9 1993 This study demonstrates that glucose-induced insulin secretion is impaired by glyceraldehyde through the inactivation of glucokinase. Glyceraldehyde 78-92 glucokinase Rattus norvegicus 121-132 8431420-6 1993 Further, the enzyme purified to homogeneity by following activity with 17-hydroxyprogesterone as a substrate was shown to reduce glucose, glyceraldehyde, and benzaldehyde (all classic aldose reductase substrates). Glyceraldehyde 138-152 aldose reductase Bos taurus 184-200 8504883-0 1993 Pharmacological interference with phospholipase A2 activity reveals mechanistic differences between glucose and glyceraldehyde induced insulin release: implication for coupling of glucose metabolism to phospholipase A2 activity. Glyceraldehyde 112-126 phospholipase A2 group IB Rattus norvegicus 34-50 7906643-2 1993 The possibility that 8-bromo cyclic adenosine monophosphate (8-Br-cAMP) or acetylcholine (ACh) potentiates insulin release in chicken pancreas in response to D-glyceraldehyde (D-GA, a weak insulinotropic fuel), and permits an insulin release in response to D-mannose or alpha-ketoisocaproic acid (alpha-KIC) (two non-insulinotropic fuels in chicken pancreas) is examined. Glyceraldehyde 158-174 insulin Gallus gallus 107-114 7906643-4 1993 8-Br-cAMP (1 mM) or ACh (1 microM) permitted a sustained although delayed insulin release in response to D-GA (5 and 15 mM). Glyceraldehyde 119-123 insulin Gallus gallus 88-95 1499867-3 1992 When the aldose reductase (DL-glyceraldehyde-reducing) activity was analyzed in mesangial cell extract, the Lineweaver-Burk plot showed concave downward curvature, and the Michaelis constant was 0.83 mM DL-glyceraldehyde, and this activity was noncompetitively inhibited by an aldose reductase inhibitor, ICI-128,436. Glyceraldehyde 29-44 aldo-keto reductase family 1 member B1 Rattus norvegicus 9-25 8412503-1 1993 Glucokinase activity in pancreatic islets was dose-dependently inactivated by D-glyceraldehyde, whereas islet hexokinase activity was not altered. Glyceraldehyde 78-94 glucokinase Homo sapiens 0-11 8412503-3 1993 However, glyceraldehyde highly attenuated the insulin-secretory response of pancreatic islets to alpha-D-glucose compared with that to beta-D-glucose. Glyceraldehyde 9-23 insulin Homo sapiens 46-53 8412503-6 1993 Our study suggests that defective discrimination of glucose anomers by glyceraldehyde-treated islets may be caused by inactivation of glucokinase. Glyceraldehyde 71-85 glucokinase Homo sapiens 134-145 1417791-2 1992 Glyceraldehyde, lactate and dihydroxyacetone decreased pHi, but only the first two released insulin. Glyceraldehyde 0-14 glucose-6-phosphate isomerase Rattus norvegicus 55-58 1499867-3 1992 When the aldose reductase (DL-glyceraldehyde-reducing) activity was analyzed in mesangial cell extract, the Lineweaver-Burk plot showed concave downward curvature, and the Michaelis constant was 0.83 mM DL-glyceraldehyde, and this activity was noncompetitively inhibited by an aldose reductase inhibitor, ICI-128,436. Glyceraldehyde 29-44 aldo-keto reductase family 1 member B1 Rattus norvegicus 277-293 1499867-3 1992 When the aldose reductase (DL-glyceraldehyde-reducing) activity was analyzed in mesangial cell extract, the Lineweaver-Burk plot showed concave downward curvature, and the Michaelis constant was 0.83 mM DL-glyceraldehyde, and this activity was noncompetitively inhibited by an aldose reductase inhibitor, ICI-128,436. Glyceraldehyde 27-44 aldo-keto reductase family 1 member B1 Rattus norvegicus 9-25 1499867-3 1992 When the aldose reductase (DL-glyceraldehyde-reducing) activity was analyzed in mesangial cell extract, the Lineweaver-Burk plot showed concave downward curvature, and the Michaelis constant was 0.83 mM DL-glyceraldehyde, and this activity was noncompetitively inhibited by an aldose reductase inhibitor, ICI-128,436. Glyceraldehyde 27-44 aldo-keto reductase family 1 member B1 Rattus norvegicus 277-293 1596516-7 1992 The carbohydrate insulin secretagogues mannose and D-glyceraldehyde have also been found to induce islet PGE2 release, but the non-secretagogue carbohydrates L-glucose and lactate do not. Glyceraldehyde 51-67 insulin Homo sapiens 17-24 1534409-6 1992 The utility of this assay was shown by three test systems: glycerol kinase plus D-glyceraldehyde acting as an ATPase and actin-activated myosin ATPase, and myosin subfragment 1, hydrolyzing a single turnover of ATP, releasing P(i) with a rate constant the same as the steady-state ATPase activity. Glyceraldehyde 80-96 dynein axonemal heavy chain 8 Homo sapiens 110-116 1551865-2 1992 Steady state kinetic analysis at pH 7.0 of the reduction of DL-glyceraldehyde by pig muscle aldose reductase showed that the enzyme follows a sequential ordered mechanism with NADPH binding first. Glyceraldehyde 60-77 aldo-keto reductase family 1 member B Sus scrofa 92-108 1823864-4 1991 The in vitro aldose reductase reaction, which we have shown is caused by glyceraldehyde-stimulated free-radical NADPH oxidation, is inhibited by the potential anti-cataract agents, bendazac acid and bendazac lysine; these compounds also inhibit ferricytochrome c reduction in the presence of DL-glyceraldehyde and scavenge superoxide radicals. Glyceraldehyde 73-87 aldo-keto reductase family 1 member B Homo sapiens 13-29 1748675-7 1991 The mutant aldose reductase (hARK262 greater than M) shows a 66-fold increase in Km for NADPH with respect to the wild type (1.9 +/- 0.4 microM versus 125 +/- 14 microM), whereas the Km for DL-glyceraldehyde increased 35-fold (20 +/- 2 versus 693 +/- 41 microM). Glyceraldehyde 190-207 aldo-keto reductase family 1 member B Homo sapiens 11-27 1902671-0 1991 Enantiospecific change in products for aldose reductase-mediated reaction of glyceraldehyde with bound NADP+. Glyceraldehyde 77-91 aldo-keto reductase family 1 member B Homo sapiens 39-55 1902671-1 1991 Aldose reductase-mediated reaction of glyceraldehyde with enzyme-bound NADP+ gives different products depending on the enantiomer used. Glyceraldehyde 38-52 aldo-keto reductase family 1 member B Homo sapiens 0-16 1900532-4 1991 Inhibition of aldose reductase was mixed type for glyceraldehyde (Ki = 8.0 x 10(-8) M) and noncompetitive for NADPH (Ki = 1.70 x 10(-8) M). Glyceraldehyde 50-64 aldo-keto reductase family 1 member B1 Rattus norvegicus 14-30 1368496-2 1992 While both PTXR and rat lens AR are NADPH-specific enzymes and have an affinity for a variety of substrates such as D-xylose, D,L-glyceraldehyde, and 4-nitrobenzaldehyde, the enzymes differ in their substrate affinity profiles. Glyceraldehyde 126-144 aldo-keto reductase family 1 member B1 Rattus norvegicus 29-31 1347743-1 1992 This study examines the effects of donor age on exogenous somatostatin inhibition of insulin secretion stimulated by 10 mM D-glyceraldehyde and by 20 mM beta-D-glucose in isolated perfused rat pancreas. Glyceraldehyde 123-139 somatostatin Homo sapiens 58-70 1347743-1 1992 This study examines the effects of donor age on exogenous somatostatin inhibition of insulin secretion stimulated by 10 mM D-glyceraldehyde and by 20 mM beta-D-glucose in isolated perfused rat pancreas. Glyceraldehyde 123-139 insulin Homo sapiens 85-92 1347743-2 1992 Both 6 and 30 nM synthetic somatostatin-14 affect both glyceraldehyde- and glucose-stimulated insulin secretion to a greater degree in pancreases from old animals (24-27 months) than in those from young (2-5 months). Glyceraldehyde 55-69 somatostatin Homo sapiens 27-39 1347743-2 1992 Both 6 and 30 nM synthetic somatostatin-14 affect both glyceraldehyde- and glucose-stimulated insulin secretion to a greater degree in pancreases from old animals (24-27 months) than in those from young (2-5 months). Glyceraldehyde 55-69 insulin Homo sapiens 94-101 1505854-4 1992 KJE and HJE inhibited aldose reductase activity, when DL-glyceraldehyde was used as substrate, with IC50 values of 2.68 x 10(-5) g/ml and 4.45 x 10(-5) g/ml, respectively and when D-glucose was used as substrate, with IC50 values of 1.04 x 10(-4) g/ml and 1.55 x 10(-4) g/ml, respectively. Glyceraldehyde 54-71 aldo-keto reductase family 1 member B Homo sapiens 22-38 1727727-0 1992 Activation of phospholipase D by glyceraldehyde in isolated islet cells follows protein kinase C activation. Glyceraldehyde 33-47 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 14-29 1727727-4 1992 Experimental confirmation of a concentration-dependent specific activation of PLD was provided by the formation of a transphosphatidylation product, phosphatidylethanol, after stimulation with glyceraldehyde in the presence of added ethanol (1.5%). Glyceraldehyde 193-207 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 78-81 1727727-9 1992 The finding of an early rise in glyceraldehyde-stimulated diacylglycerol (which may be formed de novo or by the action of phospholipase C), suggests that PLD is recruited by the activation of protein kinase C by this nutrient. Glyceraldehyde 32-46 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 154-157 1836354-4 1991 The autoxidation of glyceraldehyde in imidazole-glycylglycine buffer, measured by oxygen consumption, depends on the buffer concentration and decreases in the presence of superoxide dismutase and catalase. Glyceraldehyde 20-34 catalase Homo sapiens 196-204 1836354-6 1991 When human red-blood-cell membranes are incubated with glyceraldehyde, the red-blood-cell ATPase activities decrease significantly. Glyceraldehyde 55-69 dynein axonemal heavy chain 8 Homo sapiens 90-96 1836354-8 1991 Methylglyoxal (a dicarbonyl which is analogous to hydroxypyruvaldehyde derived from glyceraldehyde autoxidation) proved to have a powerful inhibitory action on ATPase activities. Glyceraldehyde 84-98 dynein axonemal heavy chain 8 Homo sapiens 160-166 1823864-4 1991 The in vitro aldose reductase reaction, which we have shown is caused by glyceraldehyde-stimulated free-radical NADPH oxidation, is inhibited by the potential anti-cataract agents, bendazac acid and bendazac lysine; these compounds also inhibit ferricytochrome c reduction in the presence of DL-glyceraldehyde and scavenge superoxide radicals. Glyceraldehyde 292-309 aldo-keto reductase family 1 member B Homo sapiens 13-29 2210070-5 1990 CHX also impaired insulin secretion induced by D-glyceraldehyde and dimethyl succinate, which are believed to stimulate the release of the hormone by being directly oxidized by glyceraldehyde-3-phosphate dehydrogenase, by entering the midstream of the glycolytic pathway as glyceraldehyde 3-phosphate, or by entering the tricarboxylic acid cycle in mitochondria after intracellular hydrolysis. Glyceraldehyde 47-63 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 177-217 2174432-5 1990 Aldose reductase is isolated in one of two forms that are distinguishable by their kinetic patterns with glyceraldehyde as substrate and which are interconvertible by treatment with dithiothreitol. Glyceraldehyde 105-119 aldo-keto reductase family 1 member B Homo sapiens 0-16 2245873-6 1990 Because glyceraldehyde, which enters metabolism at the triose phosphates in the glycolytic pathway, is a potent insulin secretagogue but pyruvate, which is metabolized in the mitochondrion, is not an insulin secretagogue, the proximal signal for glucose-induced insulin release originates with an interaction between the central part of the glycolytic pathway and mitochondrial metabolism. Glyceraldehyde 8-22 insulin Homo sapiens 112-119 2118267-5 1990 Isoliquiritigenin inhibited rat lens aldose reductase with an IC50 of 3.2 x 10(-7) M, using DL-glyceraldehyde as a substrate. Glyceraldehyde 92-109 aldo-keto reductase family 1 member B1 Rattus norvegicus 37-53 2115481-5 1990 When cells growing 24 h on 27.5 mM glucose were changed to medium containing 5.5 mM glucose, sorbitol concentration returned to the control level within 12 h. The activity of aldose reductase was increased by a factor of 1.6 by exposure to elevated glucose concentrations, and the relative reactivity of the enzyme with glucose as substrate was approximately 0.1 compared with that of glyceraldehyde as substrate. Glyceraldehyde 385-399 aldo-keto reductase family 1 member B Homo sapiens 175-191 2117925-2 1990 All aldose reductase inhibitors examined inhibited aldehyde reductase to some extent both in the reductive reaction as determined with glyceraldehyde as substrate and NADPH as coenzyme, and in the oxidative reaction where L-gulonic acid was oxidized to D-glucuronic acid in the presence of NADP+. Glyceraldehyde 135-149 aldo-keto reductase family 1 member B1 Rattus norvegicus 4-20 2117925-2 1990 All aldose reductase inhibitors examined inhibited aldehyde reductase to some extent both in the reductive reaction as determined with glyceraldehyde as substrate and NADPH as coenzyme, and in the oxidative reaction where L-gulonic acid was oxidized to D-glucuronic acid in the presence of NADP+. Glyceraldehyde 135-149 aldo-keto reductase family 1, member B7 Rattus norvegicus 51-69 2117925-6 1990 Marked differences in the selectivity of these inhibitors, expressed as the ratio of IC50 values for rat kidney aldehyde reductase versus rat lens aldose reductase with glyceraldehyde as substrate, were observed with selectivity for aldose reductase ranging from ca. Glyceraldehyde 169-183 aldo-keto reductase family 1 member B1 Rattus norvegicus 147-163 2117925-6 1990 Marked differences in the selectivity of these inhibitors, expressed as the ratio of IC50 values for rat kidney aldehyde reductase versus rat lens aldose reductase with glyceraldehyde as substrate, were observed with selectivity for aldose reductase ranging from ca. Glyceraldehyde 169-183 aldo-keto reductase family 1 member B1 Rattus norvegicus 233-249 2113526-9 1990 ALR2 shows normal hyperbolic kinetics with most substrates except with glyceraldehyde, which exhibits substrate activation. Glyceraldehyde 71-85 aldo-keto reductase family 1 member B Homo sapiens 0-4 2113526-10 1990 Treatment of ALR2 with dithiothreitol converted it into a form that exhibited hyperbolic kinetics with glyceraldehyde. Glyceraldehyde 103-117 aldo-keto reductase family 1 member B Homo sapiens 13-17 34138357-7 2021 In vivo studies on 4T1 tumor-bearing mouse model demonstrated that the DLG-based strategy efficiently prevented tumor recurrence and metastasis by locally reversing the immunosuppression and synergistically blocking the CD47-dependent immune escape, thereby boosting the systemic immune responses. Glyceraldehyde 71-74 CD47 antigen (Rh-related antigen, integrin-associated signal transducer) Mus musculus 220-224 2186702-7 1990 The effects of glyceraldehyde suggest that glucose signals the first phase of insulin release by an agonist-like mechanism that originates in the cytosol and requires minimal energy. Glyceraldehyde 15-29 insulin Homo sapiens 78-85 34600335-6 2021 Simulations revealed at the basal condition, NRF2 is sequestered by KEAP1 and the KEAP1-NRF2 complex is distributed comparably in an ETGE-bound (open) state and an ETGE and DLG dual-bound (closed) state. Glyceraldehyde 173-176 kelch like ECH associated protein 1 Homo sapiens 82-87 34684371-13 2021 Glyceraldehyde-derived AGE separated non-alcoholic fatty liver (NAFL) from non-alcoholic steatohepatitis (NASH) with acceptable performance (AUC 0.78). Glyceraldehyde 0-14 renin binding protein Homo sapiens 23-26 35114011-1 2022 TKFC-encoded triokinase catalyzes glyceraldehyde phosphorylation in fructose metabolism and favors lipogenesis in mice. Glyceraldehyde 34-48 triokinase, FMN cyclase Mus musculus 0-4 35408532-1 2022 This present work is designed to evaluate the anti-diabetic potential of 22 ginsenosides via the inhibition against rat lens aldose reductase (RLAR), and human recombinant aldose reductase (HRAR), using DL-glyceraldehyde as a substrate. Glyceraldehyde 203-220 aldo-keto reductase family 1 member B1 Rattus norvegicus 125-141 35408532-1 2022 This present work is designed to evaluate the anti-diabetic potential of 22 ginsenosides via the inhibition against rat lens aldose reductase (RLAR), and human recombinant aldose reductase (HRAR), using DL-glyceraldehyde as a substrate. Glyceraldehyde 203-220 aldo-keto reductase family 1 member B Homo sapiens 172-188 2699445-8 1989 Exposing the cells to 1 mM or 2 mM butyrate for two days, resulted in a 50% increase in cellular insulin content at the expense of a partial (1 mM) or complete (2 mM) loss of stimulated insulin release in response to glyceraldehyde or serine. Glyceraldehyde 217-231 insulin Homo sapiens 186-193 2518736-2 1989 Pancreatic alpha-amylase is more susceptible to inhibitory activity of d-glyceraldehyde and d-mannitol and glycerol in comparison to alpha-amylase from saliva and granulocytes. Glyceraldehyde 71-87 amylase alpha 2A Homo sapiens 0-24 3076778-5 1988 Of the nutrients tested, only glyceraldehyde produced a fall in pHi, both glucose and alpha-ketoisocaproate causing a gradual and sustained rise in pHi. Glyceraldehyde 30-44 glucose-6-phosphate isomerase Rattus norvegicus 64-67 2539042-2 1989 Glyceraldehyde has been known to be an insulin secretagogue for more than 15 years. Glyceraldehyde 0-14 insulin Homo sapiens 39-46 2539042-7 1989 These data suggest that besides stimulating insulin release in islets via its entering metabolism by phosphorylation to glyceraldehyde phosphate in the triokinase reaction, glyceraldehyde could be phosphorylated by Pi in the glyceraldehyde phosphate dehydrogenase reaction to form glycerate 1-phosphate which is probably unmetabolizable in islets. Glyceraldehyde 120-134 insulin Homo sapiens 44-51 2646171-0 1989 Delayed and atypical D-glyceraldehyde-induced insulin secretion from the perfused duodenum pancreas of chicken. Glyceraldehyde 21-37 insulin Gallus gallus 46-53 2646171-1 1989 Insulin release by the isolated-perfused pancreas of 5-8 week-old chickens was studied in response to graded concentrations of D-glyceraldehyde (D-GA) (5-20 mM). Glyceraldehyde 127-143 insulin Gallus gallus 0-7 2646171-1 1989 Insulin release by the isolated-perfused pancreas of 5-8 week-old chickens was studied in response to graded concentrations of D-glyceraldehyde (D-GA) (5-20 mM). Glyceraldehyde 145-149 insulin Gallus gallus 0-7 2646171-6 1989 Glucose (2.8 or 14 mM) sensitized the pancreas to D-GA by eliciting earlier and higher insulin response but never restored an immediate and biphasic secretory response to D-GA. Glucose amplified the response to low D-GA levels (5 and 10 mM) and inhibited the response to higher concentrations (15 and 20 mM). Glyceraldehyde 50-54 insulin Gallus gallus 87-94 3166996-3 1988 Reaction of RNase A (0.5 mM) with glyceraldehyde (20 mM) at pH 7.4 and 37 degrees C for 4 h resulted in the intermolecular cross-linking of the protein, with the concomitant development of a yellow chromophore with two new absorption bands having maxima around 305 and 375 nm. Glyceraldehyde 34-48 ribonuclease A family member 1, pancreatic Homo sapiens 12-19 3166996-9 1988 The cross-linking reaction was inhibited when the reaction of RNase A with glyceraldehyde was carried out in the presence of amino compounds, such as glycine ethyl ester, ethanolamine, glucosamine, and aminoguanidine. Glyceraldehyde 75-89 ribonuclease A family member 1, pancreatic Homo sapiens 62-69 2569024-4 1989 Somatostatin-28 and pancreatic polypeptide, both alone and in combination, reduced glucose- and glucagon-stimulated insulin release from HIT-T15 cells and glyceraldehyde- and glucagon-stimulated insulin release from RINm5F cells. Glyceraldehyde 155-169 insulin Mesocricetus auratus 195-202 2496284-4 1989 D-[6-13C]Glucose and D-[1-13C]fructose are converted directly into D-sorbitol via the aldose reductase and sorbitol dehydrogenase pathway, respectively, whereas D-[1-13C]ribose and [2-13C]glycerol give rise to labeling of the D-glyceraldehyde pool which on its turn causes a labeling of D-sorbitol. Glyceraldehyde 226-242 aldo-keto reductase family 1 member B1 Oryctolagus cuniculus 86-102 2492526-5 1989 The best substrates for ALR2 are aromatic aldehydes (e.g. pyridine-3-aldehyde; Km = 9 microM; kcat/Km = 150,000 s-1 M-1), while among aldoses DL-glyceraldehyde is the preferred substrate (Km = 72 microM; kcat/Km = 17,250). Glyceraldehyde 142-159 aldo-keto reductase family 1 member B Homo sapiens 24-28 3060124-5 1988 Stimulation of islet cells with glyceraldehyde produced a sustained fall in pHi, whereas glucose and alpha-ketoisocaproate caused a small, gradual rise in pHi. Glyceraldehyde 32-46 glucose-6-phosphate isomerase Rattus norvegicus 76-79 3076778-5 1988 Of the nutrients tested, only glyceraldehyde produced a fall in pHi, both glucose and alpha-ketoisocaproate causing a gradual and sustained rise in pHi. Glyceraldehyde 30-44 glucose-6-phosphate isomerase Rattus norvegicus 148-151 2830753-3 1987 Glyceraldehyde stimulated insulin release in a concentration dependent manner, maximum stimulation occurring at 20 mmol/l. Glyceraldehyde 0-14 insulin Homo sapiens 26-33 2452099-0 1988 Single-channel Ba2+ currents in insulin-secreting cells are activated by glyceraldehyde stimulation. Glyceraldehyde 73-87 insulin Homo sapiens 32-39 2452099-4 1988 Glyceraldehyde, a substance evoking insulin secretion from the RINm5F cells, enhances the voltage-activated Ca2+ channel opening by increasing the mean open time and decreasing the longer of the two mean shut times and also decreases the voltage threshold for channel opening. Glyceraldehyde 0-14 insulin Homo sapiens 36-43 3128169-1 1988 The kinetic mechanism of NADPH-dependent aldehyde reductase II and aldose reductase, purified from human placenta, has been studied using L-glucuronate and DL-glyceraldehyde as their respective substrates. Glyceraldehyde 156-173 aldo-keto reductase family 1 member B Homo sapiens 67-83 3933003-4 1985 The activated form of aldose reductase exhibited monophasic kinetics with both glyceraldehyde and glucose (Km of glucose = 0.68 mM and Km of glyceraldehyde = 0.096 mM), whereas the native (unactivated) enzyme exhibited biphasic kinetics (Km of glucose = 9.0 and 0.9 mM and Km of glyceraldehyde = 1.1 and 0.14 mM). Glyceraldehyde 79-93 aldo-keto reductase family 1 member B Homo sapiens 22-38 3100369-3 1987 The activities of two polyol pathway enzymes, aldose reductase and sorbitol dehydrogenase, were clearly detected in the crude homogenate of cultured mesangial cells at higher levels than those of whole glomeruli when DL-glyceraldehyde or D-fructose was used as substrate. Glyceraldehyde 217-234 aldo-keto reductase family 1 member B1 Rattus norvegicus 46-62 3100369-3 1987 The activities of two polyol pathway enzymes, aldose reductase and sorbitol dehydrogenase, were clearly detected in the crude homogenate of cultured mesangial cells at higher levels than those of whole glomeruli when DL-glyceraldehyde or D-fructose was used as substrate. Glyceraldehyde 217-234 sorbitol dehydrogenase Rattus norvegicus 67-89 3091112-7 1986 In contrast to D-glucose, 10 mM of D-glyceraldehyde decreased pHi by 0.09 units, an effect persisting even in the presence of D-600. Glyceraldehyde 35-51 glucose-6-phosphate isomerase 1 Mus musculus 62-65 3091112-8 1986 From the present study it is evident that D-glyceraldehyde and D-glucose have opposite effects on pHi in pancreatic beta-cells. Glyceraldehyde 42-58 glucose-6-phosphate isomerase 1 Mus musculus 98-101 3083202-5 1986 Partially purified AR (by DE-52) from human erythrocytes expresses biphasic kinetics with glucose and glyceraldehyde. Glyceraldehyde 102-116 aldo-keto reductase family 1 member B Homo sapiens 19-21 3082363-3 1986 Native enzyme showed biphasic kinetics with substrates (glucose and glyceraldehyde), was strongly inhibited by 15 microM ADP, 1,3-diphosphoglycerate, 2,3-diphosphoglycerate and 3-phosphoglycerate, and aldose reductase inhibitors such as sorbinil and alrestatin. Glyceraldehyde 68-82 aldo-keto reductase family 1 member B Homo sapiens 201-217 3930326-2 1985 The activated form of aldose reductase exhibited monophasic kinetics with glucose and glyceraldehyde, whereas the unactivated or native enzyme exhibited a biphasic kinetics with both the substrates. Glyceraldehyde 86-100 aldo-keto reductase family 1 member B Homo sapiens 22-38 3651395-12 1987 Reductive dihydroxypropylation of amino groups of RNase A resulted in the loss of its enzyme activity, the extent of inactivation increasing with the concentration of the glyceraldehyde used. Glyceraldehyde 171-185 ribonuclease A family member 1, pancreatic Homo sapiens 50-57 3083781-3 1986 In an NADPH-supported reduction reaction, aldose reductase exhibited similar activity toward benzaldehyde and glyceraldehyde, but benzyl alcohol was a much better substrate than physiological polyols in the analog-dependent oxidation reaction: relative kcat/Km ratios were 740 for benzyl alcohol, 2.2 for xylitol, and 1.0 for glycerol. Glyceraldehyde 110-124 aldo-keto reductase family 1 member B1 Rattus norvegicus 42-58 3933003-4 1985 The activated form of aldose reductase exhibited monophasic kinetics with both glyceraldehyde and glucose (Km of glucose = 0.68 mM and Km of glyceraldehyde = 0.096 mM), whereas the native (unactivated) enzyme exhibited biphasic kinetics (Km of glucose = 9.0 and 0.9 mM and Km of glyceraldehyde = 1.1 and 0.14 mM). Glyceraldehyde 141-155 aldo-keto reductase family 1 member B Homo sapiens 22-38 3933003-4 1985 The activated form of aldose reductase exhibited monophasic kinetics with both glyceraldehyde and glucose (Km of glucose = 0.68 mM and Km of glyceraldehyde = 0.096 mM), whereas the native (unactivated) enzyme exhibited biphasic kinetics (Km of glucose = 9.0 and 0.9 mM and Km of glyceraldehyde = 1.1 and 0.14 mM). Glyceraldehyde 141-155 aldo-keto reductase family 1 member B Homo sapiens 22-38 3922304-4 1985 Substrate specificity studies showed that aldose reductase, besides catalyzing the reduction of various aldehydes such as propionaldehyde, pyridine-3-aldehyde and glyceraldehyde, utilizes aldo-sugars such as glucose and galactose. Glyceraldehyde 163-177 aldo-keto reductase family 1 member B Homo sapiens 42-58 2867149-4 1985 A significant decrease in AR activity in old rats was found in midbrain (16%), brainstem (19%) and hypothalamus (19%) with D-xylose, and in midbrain (13%) with DL-glyceraldehyde. Glyceraldehyde 160-177 aldo-keto reductase family 1, member B7 Rattus norvegicus 26-28 2867149-5 1985 A significant decrease in AR activity in old rats was found in kidney with p-nitrobenzaldehyde (30%), D-xylose (31%), DL-glyceraldehyde (33%), pyridine 3-aldehyde (27%) and in duodenum with p-nitrobenzaldehyde (21%), but a significant increase was found in duodenum with pyridine 3-aldehyde (29%). Glyceraldehyde 118-135 aldo-keto reductase family 1, member B7 Rattus norvegicus 26-28 6373505-1 1984 Aldehyde reductase (AR) activity was measured in the brain, liver and heart of 23- to 26-month-old and 3-month-old male Wistar rats, using 5 substrates (p-nitrobenzaldehyde, D-glucuronate, D-xylose, DL-glyceraldehyde and pyridine 3-aldehyde). Glyceraldehyde 199-216 aldo-keto reductase family 1, member B7 Rattus norvegicus 20-22 2862249-3 1985 A significant increase of AR activity with D-xylose (67%), DL-glyceraldehyde (64%), D-glucuronate (43%) and D-glucose (21%) was found in the eye of old rats. Glyceraldehyde 59-76 aldo-keto reductase family 1, member B7 Rattus norvegicus 26-28 2985042-4 1985 Nucleotide-binding proteins enhanced NADPH oxidation induced by DL-glyceraldehyde, up to 10.6-fold with glucose-6-phosphate dehydrogenase. Glyceraldehyde 64-81 glucose-6-phosphate dehydrogenase Homo sapiens 104-137 6743693-3 1984 Glyceraldehyde autoxidises in the cellular incubations, consuming oxygen and producing glyoxalase I- and II-reactive materials. Glyceraldehyde 0-14 glyoxalase I Homo sapiens 87-99 6711801-6 1984 Thus, the modification at Lys-16 of the alpha-chain is a major factor in the inhibition of sickling by glyceraldehyde. Glyceraldehyde 103-117 Fc gamma receptor and transporter Homo sapiens 40-51 6373505-5 1984 A significant increase of AR activity of old rats was also found in liver with D-glucuronate (10%), DL-glyceraldehyde (23%) and pyridine 3-aldehyde (30%), and in heart with p-nitrobenzaldehyde (42%) and DL-glyceraldehyde (20%). Glyceraldehyde 100-117 aldo-keto reductase family 1, member B7 Rattus norvegicus 26-28 6373505-5 1984 A significant increase of AR activity of old rats was also found in liver with D-glucuronate (10%), DL-glyceraldehyde (23%) and pyridine 3-aldehyde (30%), and in heart with p-nitrobenzaldehyde (42%) and DL-glyceraldehyde (20%). Glyceraldehyde 203-220 aldo-keto reductase family 1, member B7 Rattus norvegicus 26-28 6404249-3 1983 High glyceraldehyde:glucuronic acid activity ratios, a characteristic of aldose reductase, were found in all lenses, except from mouse. Glyceraldehyde 5-19 aldo-keto reductase family 1, member B3 (aldose reductase) Mus musculus 73-89 6816289-6 1982 Homotropic cooperativity for both NADPH and glyceraldehyde, as evidenced by a downward curvature in the Lineweaver-Burk double-reciprocal plots, had been demonstrated for aldose reductase obtained from bovine lens (Sheaff, C.M. Glyceraldehyde 44-58 aldose reductase Bos taurus 171-187 7293231-9 1981 The high activity of epoxide hydratase towards DGEBPA suggests that glyceraldehyde and not glycidaldehyde is formed in vivo. Glyceraldehyde 68-82 epoxide hydrolase 2, cytoplasmic Mus musculus 21-38 6808090-5 1982 However, sorbinil inhibition of aldose reductase is uncompetitive with respect to glyceraldehyde and noncompetitive with NADPH as the varied substrate. Glyceraldehyde 82-96 aldo-keto reductase family 1 member B Homo sapiens 32-48 6285247-6 1982 From glyceraldehyde, glycerol (aldose reductase) or glycerate (aldehyde dehydrogenase) can be formed. Glyceraldehyde 5-19 aldose reductase Bos taurus 31-47 7045829-4 1981 GIP was also shown to potentiate insulin release initiated by D-glyceraldehyde, L-leucine/L-glutamine and 2-keto-isocaproic acid. Glyceraldehyde 62-78 gastric inhibitory polypeptide Homo sapiens 0-3 6773519-4 1980 Aldose reductase exhibited a high affinity for DL-glyceraldehyde (Km of 62 microM) and a low affinity (Km of 90 mM) for glucose, the physiological substrate of the polyol pathway. Glyceraldehyde 47-64 aldo-keto reductase family 1 member B Homo sapiens 0-16 35157-6 1979 Initial-velocity analysis and product-inhibition data revealed that pig kidney aldehyde reductase follows an Ordered Bi Bi reaction mechanism in which NADPH binds first before D-glyceraldehyde. Glyceraldehyde 176-192 aldo-keto reductase family 1 member B Sus scrofa 79-97