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the well-known interaction between AIP and 2 different isoforms of phosphodiesterases (PDEs), PDE2A3 and PDE4A5, is of particular interest. While the interaction with over-expressed AIP does not seem to affect PDE2A3 function, the reported effect on PDE4A5 is, in contrast, reduced enzymatic activity.
Lu AF33241 represents a novel PDE2A/PDE10A inhibitor tool which can penetrate the blood brain barrier.
Epigenetic regulation of phosphodiesterases 2A and 3A underlies compromised beta-adrenergic Signaling in an induced pluripotent stem cell model of dilated cardiomyopathy.
curcumin exerts its in vitro anti-angiogenic and in vivo anti-tumour properties through combined PDE2 and PDE4 inhibition
PDE2A is involved in growth and invasion of human malignant melanoma PMP cells.
This study reports the X-ray crystal structure of PDE2A in complex with a highly selective, nanomolar inhibitor (BAY60-7550) at 1.9 A resolution, and the structure of apo PDE2 at 2.0 A resolution.
PDE2 overexpression in healthy cardiomyocytes reduces the rise in cyclic AMP levels and L-type calcium current amplitude, and abolishes the inotropic effect following acute beta-adrenergic receptor stimulation.
Our results demonstrated that the PDE2A2 variant carrying point mutations is expressed in PMP cells and may affect cell cycle progression by modulating cyclin A expression.
found in smooth muscle wall of blood vessels transversing the clitoral supepithelial and stromal space
Active site similarity between human and Plasmodium falciparum phosphodiesterases: considerations for antimalarial drug design
the phosphodiesterase 2A isoform localized to mitochondria regulates respiration
Inhibition of PDE2 resulted in higher levels of intracellular cAMP than inhibition of PDE3A suggesting this PDE may be the more important regulator of cAMP in human platelets.
TNF-alpha-mediated up-regulation of PDE2 may destabilize endothelial barrier function in sepsis
Phosphodiesterase 2 mediates redox-sensitive endothelial cell proliferation and angiogenesis by thrombin via Rac1 and NADPH oxidase 2.
report the X-ray crystal structures of a PDE protein that includes both catalytic and regulatory domains, namely, PDE2A containing the N-terminal GAF domains and the catalytic domain.
Cardiac hypertrophy is inhibited by a local pool of cAMP regulated by PDE2A.
Effect of PDE2 inhibition on stress-induced memory impairment is potentially mediated via modulation of neuroplasticity-related NMDAR-CaMKII-cGMP/cAMP signaling.
We conclude that increased AM PDE2A is an important negative regulator of macrophage iNOS expression.
results demonstrate strong presynaptic inhibition by natriuretic peptides in the brain and suggest important physiological and behavioral roles of PDE2A in modulating neurotransmitter release
cGMP binding to PDE2 GAF-B activates the enzyme rapidly, stoichiometrically, and in an all or none fashion, rather than variably over a large range of cyclic nucleotide concentrations
HV(T)-induced endothelial barrier dysfunction resulted from a simultaneous increase in NO/sGC-derived cGMP and PDE2A expression causing decreased cAMP.
dual acylation as mechanism targeting neuronal PDE2A3 to synapses thereby ensuring local control of cyclic nucleotides.
activation induces decreased cAMP accumulation\; involved in nitric oxide mediated signaling in cardiac fibroblasts
phosphodiesterase 2A, cGMP-stimulated
, cGMP-dependent 3',5'-cyclic phosphodiesterase
, phosphodiesterase 2A
, cGMP-dependent 3',5'-cyclic phosphodiesterase-like
, cGMP-stimulated phosphodiesterase 1
, cGMP-stimulated phosphodiesterase 4
, cyclic GMP-stimulated phosphodiesterase
, cyclic GMP stimulated phosphodiesterase
, c-GMP stimulated phosphodiesterase