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

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.

7. Overexpression of PDE5 in papillary thyroid carcinomas.

8. cGMP PDE 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.

11. inhibition of PDE5 can counteract apoptosis during aging by modulating proand antiapoptotic molecules and the APP pathway.

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

13. it is concluded that assessment of PDE5 and PDE9 expression may be useful in the differential diagnosis of benign and malignant breast disease and successful treatment of breast cancer

14. analysis of amino acid residues responsible for the selectivity of tadalafil binding to two closely related phosphodiesterases, PDE5 and PDE6

15. PDE5 is highly expressed and increases ( approximately 130%) during growth whereas ABCC5 exhibited low to moderate expression, with a moderate increase ( approximately 40%) during growth

16. PDE9 is widely distributed in the urothelial epithelium of the human lower urinary tract and its potential roles may be different from those of PDE5.

17. Treatment of L-1236 with PDE5A-inhibitor sildenafil or with siRNA directed against PDE5A and concomitant stimulation with cyclic guanosine monophosphate (cGMP) resulted in enhanced apoptosis, indicating PDE5A as an oncogene.

18. found in smooth muscle wall of blood vessels transversing the clitoral supepithelial and stromal space

19. PDE5 inhibition by sulindac sulfide selectively induces apoptosis and attenuates oncogenic Wnt/beta-catenin-mediated transcription in human breast tumor cells

20. the spatial localization of PDE5A at the level of caveolin-rich lipid rafts allows for a feedback loop between endothelial PDE5A and nitric oxide synthase (NOS3)

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

1. analysis of the mechanisms involved revealed the induction of bone morphogenetic protein-7 (BMP7) expression, a critical regulator of angiogenesis and kidney homeostasis, through a PDE5i-dependent downregulation of miR-22. In conclusion PDE5i slows the progression of Diabetic Nephropathy (DN) in mice, improving hemodynamic parameters and vessel integrity.

2. 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.

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

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

5. 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 generation and increased PDE5 activity.

6. Inhibition of type 5 phosphodiesterase counteracts beta2-adrenergic signalling in beating cardiomyocytes.

7. 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.

8. findings reveal that excess adenosine-mediated ADORA2B signaling underlies reduced penile PDE activity by decreasing PDE5 gene expression in a HIF-1alpha-dependent manner

9. Phosphodiesterase 5 attenuates the vasodilatory response in renovascular hypertension.

10. Findings suggest that continuous, long-term treatment with PDE5 inhibitors reverses eNOS uncoupling in the sickle cell penis which restores endothelial NO synthesis.

11. 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.

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

13. PDE5 inhibition did not alter atrial natriuretic peptide-stimulated cGMP in the resting heart but augmented it in the transaortic constriction heart.

14. Sildenafil-mediated PDE5 inhibition significantly reduces diaphragm respiratory muscle dysfunction and pathology in the mdx mouse model of Duchenne muscular dystrophy.

15. these data strongly support a primary role of myocyte PDE5 regulation to myocardial pathobiology

16. PDE5-inhibition blocks TRPC6 channel activation and associated Cn/NFAT activation signaling by PKG-dependent channel phosphorylation

17. PDE5 inhibition enhances ischemia-induced angiogenesis with mobilization of endothelial progenitor cells through a protein kinase G-dependent HIF-1/vascular endothelial growth factor pathway.

18. phosphorylation and functional suppression of TRPC6 underlie prevention of pathological hypertrophy by PDE5 inhibition.

19. Myocardial oxidative stress increases PDE5 expression in the failing heart

20. Data show that recombinant cyclic GMP-binding phosphodiesterase 5 (PDE5) is activated directly upon cGMP binding to the GAF A domain, and this effect does not require PDE5 phosphorylation.

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

1. ectopic expression of bovine phosphodiesterase 5 in Drosophila has shown that it has a critical role in Malpighian (renal) tubule function in vivo and that function is conserved across evolution

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

1. Phosphodiesterase-5 activity exerts a vasoconstrictor influence on coronary resistance vessels that is mediated, in part, via an increase in endothelial endothelin production.

2. 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 receptor blockade in the presence of PDE5 inhibition.

3. Endothelial dysfunction enhances the pulmonary and systemic vasodilator effects of phosphodiesterase-5 inhibition in awake swine at rest and during treadmill exercise

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