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Lung Phosphodiesterase Isoenzymes
1993The distinct phosphodiesterase isoenzyme activities in guinea-pig lung were identified and characterised. We demonstrate that protein kinase A catalyses the activation of lung Type V cyclic GMP phosphodiesterase. This occurs via a marked change in the Vmax for cyclic GMP hydrolysis.
Pyne, N J, Burns, F
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Cyclic nucleotide phosphodiesterases
Journal of Allergy and Clinical Immunology, 2001Cyclic nucleotide second messengers (cAMP and cGMP) play a central role in signal transduction and regulation of physiologic responses. Their intracellular levels are controlled by the complex superfamily of cyclic nucleotide phosphodiesterase (PDE) enzymes. Continuing advances in our understanding of the molecular pharmacology of these enzymes has led
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Tyrosyl‐DNA Phosphodiesterase (Tdp1) (3′‐Phosphotyrosyl DNA Phosphodiesterase)
2006Tyrosyl-DNA phosphodiesterase (Tdp1) hydrolyzes 3'-phosphotyrosyl bonds in vitro. Because topoisomerase I, a type IB topoisomerase, is the only enzyme known to form 3'-phosphotyrosine bonds in eukaryotic cells, it was proposed that Tdp1 is involved in the repair of dead-end topoisomerase I-DNA covalent complexes that may form in vivo.
Amy C, Raymond, Alex B, Burgin
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Phosphodiesterase fromThiobacillus thioparus
Experientia, 1961La phosphodiesterase a ete isolee des cellules duTh. thioparus et partiellement purifiee. Cette enzyme hydrolise les polynucleotides jusqu'a 5′-mononucleotides. Elle est specifiquement activee par les ions du Mn++ et inhibee par les ions du Zn++. Son pH optimum est compris entre 8,5–9,0.
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2021
Cerebral ischemic diseases are among the most prevalent causes of death and the leading cause of adult disability worldwide. Although many studies have investigated the pathophysiological mechanisms involved in the cerebral ischemic injury, no effective pharmacological treatment has been established.
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Cerebral ischemic diseases are among the most prevalent causes of death and the leading cause of adult disability worldwide. Although many studies have investigated the pathophysiological mechanisms involved in the cerebral ischemic injury, no effective pharmacological treatment has been established.
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