Browse our phosphodiesterase 5A, cGMP-Specific Proteins (PDE5A)

Human phosphodiesterase 5A, cGMP-Specific (PDE5A) interaction partners

1. Thsese findings provide insight into the existence of distinct "pools" of PDE5A in human arterial smooth muscle cells and support the idea that these discrete compartments regulate distinct cGMP-dependent events.

2. The analogues showed a relative narrow range of Ki values for PDE5A inhibition (1.2-14 nm).

3. Data indicate that high type 5 phosphodiesterase (PDE5) expression in glioblastoma multiforme (GBM) cells significantly correlated with longer overall survival of patients.

4. the relationship between PDE5A polymorphisms, diabetes, and the efficacy of sildenafil treatment.The response to sildenafil treatment depends on polymorphisms in the PDE5A gene and the glycemic status of the patients.

5. Study showed that past attempts to quantify PDE5 mRNA were flawed due to the use of incorrect primers, and that when correct primers are used, PDE5 mRNA is detectable in human brain tissue; that PDE5 protein exists in human brain by western blot and ELISA; and performed immunohistochemistry and demonstrate that PDE5 is present in human neurons.

6. Our data showed a significant and previously undocumented upregulation of PDE5 in both rat and human BPH (show GLI3 Proteins).

7. Overexpression of PDE5 in papillary thyroid carcinomas.

8. cGMP PDE (show ALDH7A1 Proteins) isozymes, PDE5 and 10, are elevated in colon tumor cells compared with normal colonocytes, and inhibitors and siRNAs can selectively suppress colon tumor cell growth

9. Results show that Ser102 and Ser104 may influence the conformational flexibility of PDE5A, which may in turn influence phosphorylation status, allosteric regulation by cGMP or other as yet unknown regulatory mechanisms for PDE5A.

10. PDE5A appears to jointly influence amygdala volume and emotion recognition performance.

Mouse (Murine) phosphodiesterase 5A, cGMP-Specific (PDE5A) interaction partners

1. the activation of PDE5 is among the mechanisms contributing to the cGMP decrease, these results suggest that another cGMP phosphodiesterase is also activated by LH signaling.

2. Report expression of Pde5a1/2/3 in cardiac myocytes and suggest role in induction of cardiac hypertrophy.

3. Upon S-nitrosylation, PDE5 exhibits reduced activity and degradation via the ubiquitin-proteasome system.

4. Short-term hemolysis is sufficient to establish a priapism phenotype and results in loss of erectile function. PDE5I treatment ameliorates priapism, in part, because of restored NO balance with decreased ROS (show ROS1 Proteins) generation and increased PDE5 activity.

5. Addition of sildenafil, a phosphodiesterase 5 (PDE5) inhibitor, in the drinking water had a small effect in reducing myocyte hypertrophy in wild type mice and no effect in betaRM mice.

6. findings reveal that excess adenosine-mediated ADORA2B (show ADORA2B Proteins) signaling underlies reduced penile PDE (show TWIST1 Proteins) activity by decreasing PDE5 gene expression in a HIF-1alpha (show HIF1A Proteins)-dependent manner

7. Findings suggest that continuous, long-term treatment with PDE5 inhibitors reverses eNOS (show NOS3 Proteins) uncoupling in the sickle cell penis which restores endothelial NO synthesis.

8. Data indicate that the phosphodiesterase 5 (PDE5) expression is equal in the splenocytes from both genders, but splenocytes from female mice possess higher basal level of cGMP compared to the male ones.

9. Myocardial PDE5 expression is increased in the hearts of humans and mice with chronic pressure overload.

10. PDE5 inhibition did not alter atrial natriuretic peptide (show NPPA Proteins)-stimulated cGMP in the resting heart but augmented it in the transaortic constriction heart.

Cow (Bovine) phosphodiesterase 5A, cGMP-Specific (PDE5A) interaction partners

Pig (Porcine) phosphodiesterase 5A, cGMP-Specific (PDE5A) interaction partners

1. PDE5 inhibition and increase in cGMP produce pulmonary vasodilation that is mediated in part through inhibition of the ET pathway, thereby precluding an additional vasodilator effect of ETA/ETB (show EDNRB Proteins) receptor blockade in the presence of PDE5 inhibition.

2. PDE5 is a key regulator of NO-induced vasodilation in the postnatal pulmonary arteries.