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Protective effect of an adenosine kinase inhibitor in septic shock.
Preclinical Pharmacokinetics of a HepDirect Prodrug of a Novel Phosphonate-Containing Thyroid Hormone Receptor Agonist
Tissue distribution and whole body autoradiography confirmed that the liver is the major target organ of MB07811 and that conversion to MB07344 was high in the liver relative to that in other tissues, an indication of an extensive hepatic first-pass effect.
Inhibition of neutrophil adhesion by adenosine and an adenosine kinase inhibitor. The role of selectins.
Interactions between L-selectin and the neutrophil cytoskeleton might be altered by adenosine and could contribute toadenosine-mediated adhesion inhibition, and synthesized inhibitors of an enzyme involved inAdenosine metabolism, Adenosine kinase (AK) (EC, to enhance endogenous adenosines concentrations at sites of inflammation.
Evidence for functional heterogeneity among the catalytic sites of the bovine heart mitochondrial F1-ATPase.
The characteristics of ATP hydrolysis at a single catalytic site of the bovine heart F1-ATPase (MF1) as originally described were compared with those of various chemically modified preparations of MF1 in which the steady state activity was severely attenuated, supported by the properties of enzyme modified by 5'-p-fluorosulfonylbenzoyladenosine.
Inhibition of the bovine-heart mitochondrial F1-ATPase by cationic dyes and amphipathic peptides.
Rhodamine 6G, rosaniline, dequalinium, melittin, Syn-A2, and Syn-C were observed to protect F1 against inactivation by the aziridinium of quinacrine mustard in accord with their experimentally determined I0.5 values.
Gene activation of SMN by selective disruption of lncRNA-mediated recruitment of PRC2 for the treatment of spinal muscular atrophy
  • C. Woo, V. Maier, +15 authors J. Barsoum
  • Biology, Medicine
    Proceedings of the National Academy of Sciences
  • 13 February 2017
It is demonstrated that the repressed state of SMN2 is reversible by interrupting the recruitment of a repressive epigenetic complex in disease-relevant cell types, providing proof-of-concept that this technology can be used to treat disease caused by epigenetic silencing of specific loci.
Adenosine-mediated inhibition of platelet aggregation by acadesine. A novel antithrombotic mechanism in vitro and in vivo.
It is demonstrated that acadesine exhibits antiplatelet activity in vitro, ex vivo, and in vivo through an adenosine-dependent mechanism, and the in vitro studies indicate that inhibition of platelet aggregation requires the presence of erythrocytes and metabolism of acadeine to acadesines monophosphate (ZMP).