EC Number   |
General Information |
Reference |
|---|
   3.1.4.53 | malfunction |
a pdeHDELTA/pdeLDELTA mutant shows reduced conidiation, exhibits dramatically increased cAMP levels relative to the wild-type, and is completely defective in virulence |
716721 |
| 3.1.4.53 | malfunction |
deletion of cpdA results in the accumulation of intracellular cAMP and altered regulation of Pseudomonas aeruginosa virulence traits |
712298 |
| 3.1.4.53 | malfunction |
deletion of cpdA results in the accumulation of intracellular cAMP and altered regulation of Pseudomonas aeruginosa virulence traits. The cpdA mutant has a cAMP-independent small-colony, slow-growth phenotype |
712298 |
| 3.1.4.53 | malfunction |
effects of acute hypoxia on cAMP accumulation induced by PDE inhibitors in oxygen-specific chemosensors, the carotid bodies and in non-chemosensitive CB-related structures: carotid arteries and superior cervical ganglia, overview. Acute hypoxia enhances the effects of IBMX and PDE4 inhibitors on cAMP accumulation in carotid arteries and bodies, while in superior cervical ganglia In SCG, acute hypoxia reduces cAMP accumulation induced by all the four PDE inhibitors |
714638 |
| 3.1.4.53 | malfunction |
in cultured smooth muscle cells, isoform PDE1C deficiency or PDE1 inhibition attenuates smooth muscle cell proliferation and migration |
750336 |
| 3.1.4.53 | malfunction |
loss of PdeH leads to increased accumulation of intracellular cAMP during vegetative and infectious growth. Furthermore, the pdeHD shows 2-3fold enhanced conidiation, precocious appressorial development, loss of surface dependency during pathogenesis, and highly reduced in planta growth and host colonization. A pdeHDELTA/pdeLDELTA mutant shows reduced conidiation, exhibits dramatically increased cAMP levels relative to the wild-type, and is completely defective in virulence |
716721 |
| 3.1.4.53 | malfunction |
PDE4 inhibition together with transforming growth factor-beta1 results in augmented PGE2 production together with increased expression of COX mRNA and protein. inhibitors may attenuate fibroblast activities that can lead to fibrosis, PDE4 inhibitors may be particularly effective in the presence of transforming growth factor-beta1-induced fibroblast stimulation |
710817 |
| 3.1.4.53 | malfunction |
PDE8B KO mice have elevated levels of urinary corticosterone in both basal and stressed conditions compared with their littermate wild-type controls. PDE8B KO mice exhibit adrenal hypersensitivity toward adrenocorticotropin. PDE8B gene ablation increases mRNA expressions of StAR protein and MC2R |
716280 |
| 3.1.4.53 | metabolism |
a transmembrane-adenylyl-cyclase-cAMP-protein kinase A cascade modulated by isoform PDE1C is critical in regulating platelet-derived growth factor -receptor-beta degradation |
750336 |
| 3.1.4.53 | metabolism |
cyclic AMP-dependent pathways mediate the communication between external stimuli and the intracellular signaling machinery, thereby influencing important aspects of cellular growth, morphogenesis and differentiation. Crucial to proper function and robustness of these signaling cascades is the strict regulation and maintenance of intracellular levels of cAMP through a fine balance between biosynthesis, by adenylate cyclases, and hydrolysis, by cAMP phosphodiesterases |
716721 |
