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{ <http://www.tkuhn.ch/bel2nanopub/RAoJYUP-1c9Nl_FFxrEWsh1tvrMYPNyKi8zS-RaAC4VVE#_2> ?p ?o ?g. }
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Selective inhibition of PDE1C, but not of PDE4, augmented glucose-stimulated insulin secretion in a dose-dependent fashion thus demonstrating that PDE1C is the major PDE counteracting glucose-dependent insulin secretion from betaTC3 cells
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