|1.||Szutowicz, Andrzej: 12 articles (10/2015 - 09/2003)|
|2.||Bielarczyk, Hanna: 9 articles (10/2015 - 09/2003)|
|3.||Pawełczyk, Tadeusz: 7 articles (04/2015 - 09/2003)|
|4.||Ronowska, Anna: 5 articles (10/2015 - 08/2006)|
|5.||Jankowska-Kulawy, Agnieszka: 4 articles (10/2015 - 10/2010)|
|6.||Rabinowitz, Joshua D: 4 articles (03/2015 - 05/2013)|
|7.||Shulman, Gerald I: 4 articles (02/2015 - 03/2006)|
|8.||Cline, Gary W: 4 articles (02/2015 - 03/2006)|
|9.||Szutowicz, A: 4 articles (08/2011 - 01/2000)|
|10.||Gul-Hinc, Sylwia: 3 articles (10/2015 - 08/2014)|
|1.||Alzheimer Disease (Alzheimer's Disease)
09/01/2006 - "A preferential loss of brain cholinergic neurons in the course of Alzheimer's disease and other encephalopathies is accompanied by a proportional impairment of acetyl-CoA synthesizing capacity in affected brains. "
05/31/1994 - "One of the most important mechanisms in the pathogenesis of senile dementia of the Alzheimer type is the marked decrease of the cerebral glucose metabolism, a cholinergic deficit, by a disturbed acetyl-CoA synthesis and a critically lowered oxidative phosphorylation. "
10/01/2003 - "The aim of the present study was to reveal whether reduced cortical cholinergic input affects the acetyl-CoA metabolism in cholinoceptive cortical target regions which may play a causative role for the deficits in cerebral glucose metabolism observed in Alzheimer's disease. "
10/27/2015 - "AβPP-Transgenic 2576 Mice Mimic Cell Type-Specific Aspects of Acetyl-CoA-Linked Metabolic Deficits in Alzheimer's Disease."
05/15/1980 - "As a possible means of investigating this problem the relationship between the activities of several enzymes which can synthesize acetyl-CoA and the cholinergic defect of Alzheimer's disease has been examined. "
04/01/1995 - "Untreated chronic hyperammonemia resulted in a decrease in acetyl-coenzyme A and an increase in the long chain acyl-coenzyme A in the liver, accompanied by an increase in total coenzyme A in the muscular tissues. "
01/01/2013 - "KIC-induced hyperammonemia improved following administration of carglumate (N-carbamyl-L-glutamic acid), which substitutes for the product of an acetyl-CoA-dependent reaction essential for urea cycle function, demonstrating an acyl-CoA-related mechanism for this complication. "
09/01/1980 - "Thus, the principal mechanism for hyperammonemia induced by these acids is depletion of liver N-acetyl glutamate, which is in turn attributable to depletion of acetyl CoA and/or competitive inhibition by propionyl and methylmalonyl CoA of N-acetyl glutamate synthetase. "
12/01/1979 - "In the search for the mechanism by which hyperammonemia complicates propionic and methylmalonic acidemia the effects of a series of acyl-coenzyme A (CoA) derivatives were studied on the activity of N-acetylglutamate synthetase in rat liver mitochondria using acetyl-CoA as substrate. "
04/01/1984 - "Valproate-induced hyperammonemia is probably the result of depletion of mitochondrial acetyl CoA and decreased production of N-acetylglutamate, the obligatory activator of the first enzyme of the urea cycle, carbamyl phosphate synthetase I. Anticonvulsant-mediated microsomal enzyme induction may also contribute."
|3.||Metabolic Diseases (Metabolic Disease)
01/01/2015 - "Acetyl-coenzyme A carboxylases (ACCs) play critical roles in the regulation of fatty acid metabolism and have been targeted for the development of drugs against obesity, diabetes and other metabolic diseases. "
01/01/1980 - "Multiple carboxylases deficiency, a recently identified metabolic disease in infants, can be cured by the administration of biotine, a cofactor of the carboxylases: pyruvate, propionyl coenzyme A (CoA), methylcrotonyl CoA, and acetyl CoA. "
10/01/1982 - "An improved method using acetyl-coenzyme A regeneration for the enzymic inactivation of aminoglycosides prior to sterility testing."
03/01/2006 - "Thus, it seemed reasonable to infer that the decrease of putative lipoamide dehydrogenase and putative acetyl-CoA synthetase in anther might prevent the conversion of pyruvate into acetyl-CoA, and as a result, the TCA cycle could no longer operate at a sufficient rate to meet all requirements in anther cells, leading to pollen sterility. "
01/28/2015 - "In this review, we focused on the recent findings related to cancer acetate/acetyl CoA metabolism. "
01/28/2015 - "Induced acetate/acetyl CoA metabolism is a notable feature that is related to fatty acid synthesis supporting tumor growth. "
01/28/2015 - "Acetate/acetyl-CoA metabolism associated with cancer fatty acid synthesis: overview and application."
09/05/2014 - "This suggests that tumor cells with Myc deregulation might be susceptible to novel therapies that limit acetyl-CoA availability. "
01/01/2014 - "Quantitative analysis of acetyl-CoA production in hypoxic cancer cells reveals substantial contribution from acetate."
|2.||Pyruvic Acid (Pyruvate)
|3.||Coenzyme A (CoA)
|4.||Glutamic Acid (Glutamate)
|5.||Acyl Coenzyme A (Acyl CoA)
|6.||propionyl-coenzyme A (propionyl-CoA)
|9.||tiglyl-coenzyme A (methylcrotonyl-CoA)
|10.||Malonyl Coenzyme A (Malonyl CoA)