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The Purine Nucleotide Cycle is a metabolic pathway in which fumarate is generated from aspartate in order to increase the concentration of Krebs cycle intermediates.〔Salway, J. G., Metabolism at a glance (3rd edition), Blackwell Publishing Ltd., Oxford, 2004, pp. 56-57〕 The pathway was first described by John Lowenstein, who demonstrated its role in increasing the rate of oxidative phosphorylation in skeletal muscle.〔Voet, D., Voet, J. G., Biochemistry (3rd Edition), John Wiley & Sons, Inc., 2004, pp. 1094-1095〕 ==Outline== The cycle is composed of three enzyme-catalysed reactions. The first stage is the deamination of the purine nucleotide Adenosine monophosphate (AMP) to form inosine monophosphate (IMP), catalysed by the enzyme AMP deaminase: :AMP + H2O → IMP + NH4+ The second stage is the formation of adenylosuccinate from IMP and the amino acid aspartate, which is coupled to the energetically favourable hydrolysis of GTP, and catalysed by the enzyme adenylosuccinate synthetase: :Aspartate + IMP + GTP → Adenylosuccinate + GDP + Pi Finally, Adenylosuccinate is cleaved by the enzyme adenylosuccinate lyase to release fumarate and regenerate the starting material of AMP: :Adenylosuccinate → AMP + Fumarate A recent study conducted by Sridharan et al. (AJP Cell Physiology, 2008, 295:C29-C37) showed that activation of HIF-1α allows cardiomyocytes to sustain mitochondrial membrane potential during anoxic stress by utilizing fumarate produced by adenylosuccinate lyase as an alternate terminal electron acceptor in place of oxygen. This mechanism should help provide protection in the ischemic heart. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「purine nucleotide cycle」の詳細全文を読む スポンサード リンク
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