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Literature summary for 2.7.4.3 extracted from

  • Dzeja, P.P.; Bast, P.; Pucar, D.; Wieringa, B.; Terzic, A.
    Defective metabolic signaling in adenylate kinase AK1 gene knock-out hearts compromises post-ischemic coronary reflow (2007), J. Biol. Chem., 282, 31366-31372.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine knock out of the major isoform adenylate kinase 1 disrupts the synchrony between inorganic phosphate turnover at ATP-consuming sites and gamma-ATP exchange at ATP synthesis sites. This reduces energetic signal communication in the post-ischemic heart. Adenylate kinase 1 gene deletion blunts vascular adenylate kinase phosphotransfer, compromises the contractility-coronary flow relationship, and precipitates inadequate coronary reflow following ischemiareperfusion. Deficit in adenylate kinase activity abrogates AMP signal generation and reduces the vascular adenylate kinase/creatine kinase activity ratio essential for the response of metabolic sensors. The sarcolemma-associated splice variant adenylate kinase 1beta facilitates adenosine production. Adenosine treatment bypasseds adenylate kinase 1 deficiency and restores post-ischemic flow to wild-type levels Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information knock out of the major isoform adenylate kinase 1 disrupts the synchrony between inorganic phosphate turnover at ATP-consuming sites and gamma-ATP exchange at ATP synthesis sites. This reduces energetic signal communication in the post-ischemic heart. Adenylate kinase 1 gene deletion blunts vascular adenylate kinase phosphotransfer, compromises the contractility-coronary flow relationship, and precipitates inadequate coronary reflow following ischemiareperfusion. Deficit in adenylate kinase activity abrogates AMP signal generation and reduces the vascular adenylate kinase/creatine kinase activity ratio essential for the response of metabolic sensors. The sarcolemma-associated splice variant adenylate kinase 1beta facilitates adenosine production. Adenosine treatment bypasseds adenylate kinase 1 deficiency and restores post-ischemic flow to wild-type levels Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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-
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Source Tissue

Source Tissue Comment Organism Textmining
heart
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Mus musculus
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