facilitates storage and use of the high energy of the adenine nucleotides, involved in maintenance of equilibrium among adenine nucleotides and maintenance of energy charge, important to energy economy of living systems
facilitates storage and use of the high energy of the adenine nucleotides, involved in maintenance of equilibrium among adenine nucleotides and maintenance of energy charge, important to energy economy of living systems
depletion of adenylate kinase 2 (AK2) by RNAi impairs adiponectin secretion in 3T3-L1 adipocytes, immunoglobulin M secretion in BCL1 cells, and the induction of the unfolded protein response during differentiation of both cell types. Depletion of AK2 results in changes in adipocyte energy homeostasis, but these effects do not detectably impair key adipocyte properties such as mitochondrial biogenesis and triglyceride storage
method for simultaneous detection of adenylate kinase isoforms directly on gel or nitrocellulose after separation by denaturing electrophoresis and electroblotting. Method allows for quantitative dection of enzyme activity from amny sources in both its reaction courses
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
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PURIFICATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
nucleotide-binding domain 1 of CFTR purified to homogeneity by nickel ion affinity chromatography, followed by Sepharose S200 gel filtration and a second nickel affinity step
method for simultaneous detection of adenylate kinase isoforms directly on gel or nitrocellulose after separation by denaturing electrophoresis and electroblotting. Method allows for quantitative dection of enzyme activity from amny sources in both its reaction courses
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
Nucleotide-binding domains of cystic fibrosis transmembrane conductance regulator, an ABC transporter, catalyze adenylate kinase activity but not ATP hydrolysis
J. Biol. Chem.
281
4058-4068
2006
Homo sapiens (P13569), Homo sapiens, Mus musculus (P26361), Mus musculus