Increased formation of methylglyoxal and protein glycation, oxidation and nitrosation in triosephosphate isomerase deficiency.
about
Dynamic rerouting of the carbohydrate flux is key to counteracting oxidative stressStructural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle DynamicsStructural basis of human triosephosphate isomerase deficiency: mutation E104D is related to alterations of a conserved water network at the dimer interfaceHydrogen sulfide releasing aspirin, ACS14, attenuates high glucose-induced increased methylglyoxal and oxidative stress in cultured vascular smooth muscle cellsProteomic analysis of rat retina in a steroid-induced ocular hypertension model: potential vulnerability to oxidative stressTemporal dynamics of glyoxalase 1 in secondary neuronal injuryGlyoxalase II of African trypanosomes is trypanothione-dependent.Plasma amino acids and metabolic profiling of dairy cows in response to a bolus duodenal infusion of leucine.Pyruvate kinase triggers a metabolic feedback loop that controls redox metabolism in respiring cellswasted away, a Drosophila mutation in triosephosphate isomerase, causes paralysis, neurodegeneration, and early deathMethylglyoxal, the dark side of glycolysisGlyoxalase I polymorphism rs2736654 causing the Ala111Glu substitution modulates enzyme activity--implications for autism.A53T-alpha-synuclein-overexpression in the mouse nigrostriatal pathway leads to early increase of 14-3-3 epsilon and late increase of GFAPPathological significance of mitochondrial glycationInhibition of enzyme activity of Rhipicephalus (Boophilus) microplus triosephosphate isomerase and BME26 cell growth by monoclonal antibodies.Methylglyoxal in food and living organisms.Degradation of functional triose phosphate isomerase protein underlies sugarkill pathology.Early mitochondrial dysfunction leads to altered redox chemistry underlying pathogenesis of TPI deficiency.Inhibition of Non-flux-Controlling Enzymes Deters Cancer Glycolysis by Accumulation of Regulatory Metabolites of Controlling StepsGlycation potentiates neurodegeneration in models of Huntington's disease.NAD+ availability and proteotoxicity.Analytical methods for 3-nitrotyrosine quantification in biological samples: the unique role of tandem mass spectrometry.Advanced glycation endproducts and their pathogenic roles in neurological disorders.Good mass spectrometry and its place in good science.Mass spectrometry and 3-nitrotyrosine: strategies, controversies, and our current perspective.Rare hereditary red blood cell enzymopathies associated with hemolytic anemia - pathophysiology, clinical aspects, and laboratory diagnosis.Glycation, Oxidation and Glycoxidation of IgG: A Biophysical, Biochemical, Immunological and Hematological study.3-Bromopyruvate induces rapid human prostate cancer cell death by affecting cell energy metabolism, GSH pool and the glyoxalase system.Methylglyoxal alters glucose metabolism and increases AGEs content in C6 glioma cells.Phenotyping of tianma-stimulated differentiated rat neuronal b104 cells by quantitative proteomics.Triosephosphate isomerase deficiency: consequences of an inherited mutation at mRNA, protein and metabolic levels.Protein modification by dicarbonyl molecular species in neurodegenerative diseases.Characterization of stress and methylglyoxal inducible triose phosphate isomerase (OscTPI) from rice.Energy metabolism, altered proteins, sirtuins and ageing: converging mechanisms?Methylglyoxal induces oxidative stress and mitochondrial dysfunction in osteoblastic MC3T3-E1 cells.Immunological detection of fructose-derived advanced glycation end-products.In vitro nonenzymatic glycation of guanosine 5'-triphosphate by dihydroxyacetone phosphate.The structural modification of DNA nucleosides by nonenzymatic glycation: an in vitro study based on the reactions of glyoxal and methylglyoxal with 2'-deoxyguanosine.Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury.Methylglyoxal-induced cytotoxicity in neonatal rat brain: a role for oxidative stress and MAP kinases.
P2860
Q21146753-A491CE17-869A-46A4-B2AC-C30E8AAC7D27Q27309025-0F5AA881-7FE6-45D0-B819-BA5C972E4DDEQ27650882-026010AC-75EB-43B2-A5C6-0189170953B5Q28539333-FD381962-7262-4D21-812C-485609D685E4Q28578850-A297EC60-158E-48FB-AE7E-E6A04C39679CQ30317530-B345308F-9A75-4D85-8097-AA4E020EBD99Q31049371-4E673944-50F5-49BB-AFD6-09B9E3DDE423Q33615740-C3BA77C9-067E-4BD3-A6D9-BBEC8080B35EQ34215123-7DCF864C-AF8A-42AE-B6FC-2245FD579819Q35056697-2B78FD58-199C-4016-B1BD-608238FF8B51Q35063131-0B8D1671-D42F-4C12-8509-5FC94EF23C15Q35112759-49C40348-3676-4590-AE65-523BE05CCF66Q35767234-378DB140-7BE6-4D51-8EE2-32B9195D828EQ36072507-0C6C102D-8CE4-4E49-A98B-98547DF4E809Q36396524-29287554-69C3-428B-9751-268796E94627Q36653426-ADF39CBF-9C19-4A18-8B66-47295131B78CQ36724350-6C4783CB-FA53-4906-97EF-718C9542A670Q36773904-8AD6C713-1A1F-45E4-8714-36F0EBA72E03Q37277390-2B93D1BD-000C-4809-AFE3-F722073ECA38Q37421997-AD46748C-441A-4FFC-811B-09102152A0F3Q37530715-45893AC5-BB8D-491C-8EA1-4FC97A667BE0Q37760069-8609008B-14BB-4DB8-99B6-FD4327B3659FQ37800424-0048FA6D-B666-4ECA-AF80-30B7D5A43F41Q38019452-4A655AF5-8A30-40E8-9C67-83C3D39775F0Q38156144-B43D6E61-D39E-408E-B1E1-AF03C58DEF88Q38205957-13AE469C-45C6-45E7-B0CF-31FD98BE65C6Q38631878-35CA1403-7BEB-4634-8BBF-88DC8D512CB4Q38946644-9DAFA172-7574-4102-94E7-2F5FD3BCEF5FQ39313466-8773F328-573B-4357-9446-079D4BE9BFA0Q39441306-456A8435-5310-465D-A3A3-465928647984Q40679294-708F8A17-5990-4476-A646-886CE8D0E006Q40973301-E3D0D614-602F-4ADF-9B30-C959EA3228F2Q41335123-3DE6C571-FBCB-4C5B-970F-27D1821741CCQ41964977-A14330D5-36C8-496A-AD21-E1BF2B79D5FCQ42811134-707DE529-7E06-4CA2-A7F1-30F0C37C0751Q43138020-E528E1E6-F921-41E8-9A16-E9AC36B2DBFDQ46367798-81A9AC7B-99CF-4D0E-88F3-479684FDA3F5Q46927087-07E5EB0B-EE80-4B9A-A165-5F54A3DA3B3AQ47813249-209782ED-E611-4FBE-8EC8-4B6FE0164589Q48178370-1B1F078C-11EA-455D-B733-BFAD83A4ED82
P2860
Increased formation of methylglyoxal and protein glycation, oxidation and nitrosation in triosephosphate isomerase deficiency.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Increased formation of methylg ...... hosphate isomerase deficiency.
@en
Increased formation of methylg ...... hosphate isomerase deficiency.
@nl
type
label
Increased formation of methylg ...... hosphate isomerase deficiency.
@en
Increased formation of methylg ...... hosphate isomerase deficiency.
@nl
prefLabel
Increased formation of methylg ...... hosphate isomerase deficiency.
@en
Increased formation of methylg ...... hosphate isomerase deficiency.
@nl
P2093
P1476
Increased formation of methylg ...... hosphate isomerase deficiency.
@en
P2093
Klára Baróti
Margit Horányi
Naila Ahmed
Nikolaos Karachalias
Roya Babaei-Jadidi
Sinan Battah
Susan Hollan
P304
P356
10.1016/J.BBADIS.2003.08.002
P577
2003-10-01T00:00:00Z