Disease relevance of Citridic acid

• Results of mutagenesis support the interpretation of the x-ray model, namely that Asp100 and His101 form an ion pair for elimination of the substrate hydroxyl and Ser642 may function as a general base for proton abstraction from citrate or isocitrate in the dehydration step and protonation of cis-aconitate in the hydration step [1].
• Experimental visceral leishmaniasis: role of trans-aconitic acid in combined chemotherapy [2].
• The Saccharomyces cerevisiae Tmt1 gene product is the yeast homologue of the Escherichia coli enzyme that catalyzes the methyl esterification of trans-aconitate, a thermodynamically favored isomer of cis-aconitate and an inhibitor of the citric acid cycle [3].
• The FAD-dependent tricarballylate dehydrogenase (TcuA) enzyme of Salmonella enterica converts tricarballylate into cis-aconitate [4].
• At tetany, the forage K, protein, digestibility, ash alkalinity, aconitic acid and total lipids increased suddenly and markedly [5].

High impact information on Citridic acid

• In contrast, when measured by the conversion of isocitrate to cis-aconitate, S711D and S711E displayed substantial activity, indicating that phosphorylation impairs the citrate but not isocitrate mode of aconitase function [6].
• We conclude from these data that, on addition of any one of the three substrates, cis-aconitate is the predominant species bound to Fea of the cluster along with solvent HxO and that cis-aconitate is bound in the citrate mode (carboxyl at C-2) [7].
• We conjugated the chemotherapy agent daunorubicin to the anti-T-cell monoclonal antibody T101 using an active ester intermediate of the acid-labile linker cis-aconitate anhydride [8].
• S-Nitrosothiols and the NONOate sper/NO plus gluthathione (GSH) activated IRE binding by IRP whereas oxyhemoglobin prevented enhancement of this binding by SIN-1/SOD and sper/NO plus GSH. cis-Aconitate, substrate, also abolished the effect of SIN-1/SOD on IRE binding by IRP [9].
• We have exploited this synchrony to determine the respective importance and hierarchy of the known triggers for differentiation (cis aconitate, temperature drop) for individual components of both differentiation and the cell cycle [10].

Chemical compound and disease context of Citridic acid

• The proton abstracted in the dehydration of [3H]citrate is transferred directly to undissociated cis-aconitate to form isocitrate without dilution, or cis-aconitate having dissociated, the tritium passes to the medium, presumably through the pool of bound protons indicated above [11].
• This enzyme, catalyzing a dehydration and rehydration of citrate, also catalyzes the elimination of HF from 3-fluorocitrate, yielding cis-aconitate and fluoride [12].
• Mutagenic investigation of flavourings: dimethyl succinate, ethyl pyruvate and aconitic acid are negative in the Salmonella/mammalian-microsome test [13].

Biological context of Citridic acid

• The TcuB protein is proposed to work in concert with TcuA to oxidize tricarballylate to cis-aconitate, which is further catabolized via the Krebs cycle [14].
• In contrast to cis-aconitate, protease treatment resulted in considerable cell death [15].
• Stumpy forms treated with trypsin differentiated synchronously and expressed procyclin with faster kinetics than when they were triggered by cis-aconitate [15].
• Furthermore, the CCA-stimulated transformation is not dependent on putrescine and can occur independently of cell division [16].

Anatomical context of Citridic acid

• 1. Citrate was oxidized by human placental mitochondria at a rate half that for isocitrate, and cis-aconitate at a rate by 20% lower as with isocitrate [17].

Associations of Citridic acid with other chemical compounds

• Nuclear magnetic resonance spectroscopy and in vitro activity assay data showed that AcnD dehydrated 2-methylcitrate and citrate to 2-methyl-cis-aconitate and cis-aconitate, respectively; AcnD also hydrated cis-aconitate [18].
• The variation in pKi with pH was determined in the case of cis,cis-muconate and cis-aconitate, both of which gave curves suggesting the importance of a group with a pKa of approximately 6.4 responsible for increasing the inhibition of the enzyme [19].
• Dissociation constants at pH 8.5 and 37 degrees C, determined from inhibitory effects on butanedione inactivation rates are: citrate, 0.74 mM; D-isocitrate, 0.33 mM: cis-aconitate, 0.52 mM; tricarballytate, 0.42 mM; trans-aconitate, 0.025 mM [20].
• Surprisingly, HACN does not show any activity when cis-aconitate is substituted for the substrate, even though other enzymes from the alpha-aminoadipate pathway can accept analogous tricarboxylic acid-cycle substrates [21].

Gene context of Citridic acid

• The cytosolic and mitochondrial aconitase activity was 64.8% or 61.0% and 20.1% or 19.4% of the total rat liver aconitase activity when cis-aconitate or isocitrate was used as substrate [22].
• Stumpy populations emanating from these infections transformed rapidly and synchronously into dividing procyclic forms when triggered with cis-aconitate and a temperature shift [23].
• Addition of citrate/cis-aconitate at 37 degrees C to bloodstream forms leads to the formation of aconitase and proline oxidase [24].
• Cell division did not occur until 30-40 h after transfer to 27 degrees C. Various characteristics of this system were examined, including the effect of the feeder layer, the type of medium, the presence of the metabolites cis-aconitate and citrate, the preadaptation period, and the trypanosome cell concentration [25].

References