Disease relevance of GLYCERIC ACID

• Primary hyperoxaluria type II (PH2) is a rare monogenic disorder that is characterized by a lack of the enzyme that catalyzes the reduction of hydroxypyruvate to D-glycerate, the reduction of glyoxylate to glycolate and the oxidation of D-glycerate to hydroxypyruvate [1].
• Crystallization and preliminary diffraction studies of hydroxypyruvate reductase (D-glycerate dehydrogenase) from Hyphomicrobium methylovorum [2].
• The plant-like c2 glycolate cycle and the bacterial-like glycerate pathway cooperate in phosphoglycolate metabolism in cyanobacteria [3].
• In the genome of the cyanobacterium Synechocystis sp. strain PCC 6803, we have identified open reading frames encoding enzymes homologous to those forming the plant-like C2 cycle and the bacterial-type glycerate pathway [3].
• A compound representing the D-glycerate terminus of the methylglucose-containing polysaccharide of Mycobacterium smegmatis [4].

High impact information on GLYCERIC ACID

• The newly identified GLYK is both structurally and phylogenetically distinct from known glycerate kinases from bacteria and animals [5].
• Transient transfection of the cDNA clone into COS cells verified that it encoded an enzyme with hydroxy-pyruvate reductase, glyoxylate reductase and D-glycerate dehydrogenase enzymatic activities [1].
• The liver bifunctional enzyme was found to catalyze the hydrolysis of glycerate 1,3-bisphosphate to glycerate 3-phosphate and inorganic phosphate [6].
• Fast atom bombardment mass spectrometry and a specific enzymatic assay with glyoxylate reductase demonstrated that the beta 82 adduct was a glycerate moiety [7].
• These results suggested that cyanobacteria metabolize phosphoglycolate by the cooperative action of the C2 cycle and the glycerate pathway [3].

Chemical compound and disease context of GLYCERIC ACID

• BACKGROUND: The primary hyperoxalurias are autosomal recessive disorders resulting from deficiency of hepatic alanine:glyoxylate aminotransferase (PHI) or D-glycerate dehydrogenase/glyoxylate reductase (PHII) [8].
• A gene (gckA) responsible for the activity of glycerate kinase has been identified within a chromosomal fragment of the serine cycle methylotroph Methylobacterium extorquens AM1 [9].
• A common regulator for the operons encoding the enzymes involved in D-galactarate, D-glucarate, and D-glycerate utilization in Escherichia coli [10].
• In a one-tube reaction that included NADH, lactate dehydrogenase, and the three E. coli enzymes, 1 mumol of D-glucarate was quantitatively converted to 1 mumol each of D-glycerate and L-lactate with concomitant utilization of 2 mumol of NADH [11].
• Glyceraldehyde 3-p dehydrogenase, glycerate 3-P kinase and enolase mutants of Escherichia coli: genetic studies [12].

Biological context of GLYCERIC ACID

• Alternately, the activated enzyme predominantly catalyzes the hydrolysis of the intermediate to two molecules of glycerate 3-phosphate [13].
• Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the reversible oxidative phosphorylation of d-glyceraldehyde 3-phosphate (GAP) into d-glycerate 1,3-bisphosphate (1,3-diPG) in the presence of NAD(+) and inorganic phosphate (P(i)) [14].
• Of the nine genes encoding proteins required for allantoin degradation, only the one encoding glyoxylate carboligase (gcl), the first enzyme of the pathway leading to glycerate, had been identified and mapped at centisome 12 on the chromosome map [15].
• Influence of glycerate on photosynthesis by wheat chloroplasts [16].
• With the decrease in the OTR, the intracellular flux values after glycerate 3-phosphate (PG3) in the gluconeogenesis pathway and the specific growth rate decreased [17].

Anatomical context of GLYCERIC ACID

• Fructose 2,6-bisphosphate in rat erythrocytes. Inhibition of fructose 2,6-bisphosphate synthesis and measurement by glycerate 2,3-bisphosphate [18].
• Not only with intact but also with osmotically shocked peroxisomes, which had retained the aggregated state of the peroxisomal matrix but lost the integrity of the boundary membrane, the rates of glycerate synthesis were as high as required for the photorespiratory cycle in vivo [19].
• Comparison of D-glycerate dehydrogenases from beef liver, beef spinal cord and hog spinal cord [20].
• Glycerate 2,3-P2 increased the Mg2+ optimum for protein synthesis by chelation of Mg2+, but Mg2+ addition did not completely reverse the inhibition, suggesting an additional site of action. eIF-2 has been used to examine the activity of casein kinase II in reticulocyte lysates in response to glycerate 2,3-P2 [21].
• Synthesis of glucose from 10 mM D-glycerate by hepatocytes isolated from rats fasted 24 h was inhibited by 3-aminopicolinate (3AP), 3-mercaptopicolinate (3MP), and aminoxyacetate (AOA) [22].

Associations of GLYCERIC ACID with other chemical compounds

• Using NMR and permethylation/hydrolysis procedures, galactose was shown to be linked alpha-glycosidically to the 3-O-position of glyceric acid [23].
• D-Glycerate dehydrogenase (GDH) catalyzes the NADH-linked reduction of hydroxypyruvate to D-glycerate [24].
• Pi, fructose 1,6-bisphosphate and glycerate 3-phosphate, all inhibitors of the synthase, increased significantly during the first 20 s (P less than 0.05-0.001), whereas muscle pH (decrease in which inhibits synthase) decreased continuously [25].
• A mentally retarded boy exhibiting both hyper-D-glyceric acidemia and hyperglycinemia and in whom a deficiency of D-glycerate dehydrogenase had previously been demonstrated was investigated to elucidate the ethiology of the glycine accumulation and its relationship to the D-glyceric acid accumulation [26].
• Conversion of glycerate to serine in intact spinach leaf peroxisomes [27].

Gene context of GLYCERIC ACID

• This cannot be achieved on human hemolysates where glycerate 1,3-P2-dependent glucose 1,2-bisphosphate synthesis is displayed only by multifunctional PGM2 isoenzymes [28].
• The dependence of the rate of GSH production on the concentration of the hexokinase inhibitors glucose 1,6-bisphosphate and glycerate 2,3-bisphosphate showed that, under conditions of oxidative stress, hexokinase was the principal determinant of flux through the shunt [29].
• A structural determinant for glycerate 3-P kinase (pgk) is located near serA [12].
• Crystal structure of a glycerate kinase (TM1585) from Thermotoga maritima at 2.70 A resolution reveals a new fold [30].
• 3. The livers from a patient with primary hyperoxaluria type 2 (D-glycerate dehydrogenase deficiency) and one with an undefined form of primary hyperoxaluria (possibly oxalate hyperabsorption) had normal AGT levels [31].

Analytical, diagnostic and therapeutic context of GLYCERIC ACID

• During organic acid screening by gas chromatography/mass spectrometry, we detected a large peak corresponding to glyceric acid in a patient's urine sample [32].
• By differential centrifugation of the homogenate and sucrose density gradient analysis, it was found that 42% and 60% of the renal glycerate kinase were localized in the cytosol and mitochondria, respectively [33].
• Lyotropic liquid crystalline phases formed from glycerate surfactants as sustained release drug delivery systems [34].
• Specimen handling for the assay of adenylates and glycerate 2, 3-bisphosphate in erythrocytes [35].
• Chiral liquid chromatography tandem mass spectrometry in the determination of the configuration of glyceric acid in urine of patients with D-glyceric and L-glyceric acidurias [36].

References