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Elk Polyclonal PDE4A Primary Antibody for CM, ICC - ABIN2750880
Farooqui, Al-Bagdadi, Houslay, Bolger, Stout, Specian, Cherry, Conti, ODonnell: Surgically induced cryptorchidism-related degenerative changes in spermatogonia are associated with loss of cyclic adenosine monophosphate-dependent phosphodiesterases type 4 in abdominal testes of rats. in Biology of reproduction 2001
Show all 37 Pubmed References
Chicken Polyclonal PDE4A Primary Antibody for CM, ICC - ABIN2747099
Uckert, Hedlund, Waldkirch, Sohn, Jonas, Andersson, Stief: Interactions between cGMP- and cAMP-pathways are involved in the regulation of penile smooth muscle tone. in World journal of urology 2005
Show all 13 Pubmed References
Human Polyclonal PDE4A Primary Antibody for CM, ICC - ABIN2747107
Valente, Vernet, Ferrini, Qian, Rajfer, Gonzalez-Cadavid: L-arginine and phosphodiesterase (PDE) inhibitors counteract fibrosis in the Peyronie's fibrotic plaque and related fibroblast cultures. in Nitric oxide : biology and chemistry 2004
Chicken Polyclonal PDE4A Primary Antibody for WB - ABIN5683758
Ale-Agha, Goy, Jakobs, Spyridopoulos, Gonnissen, Dyballa-Rukes, Aufenvenne, von Ameln, Zurek, Spannbrucker, Eckermann, Jakob, Gorressen, Abrams, Grandoch, Fischer, Köhrer, Deenen, Unfried, Altschmied et al.: CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular system-New mode of action for caffeine. ... in PLoS biology 2018
In conclusion, our data demonstrated that UFM24 inhibits oxidative burst in human neutrophils through inhibition of PDE4 activity. UFM24 also exhibited significant protection against endotoxin-induced acute lung injury (ALI)in mice. UFM24 has potential as an anti-inflammatory agent for treating neutrophilic lung damage.
PDE4 inhibition reduces neointima formation and inhibits VCAM-1 expression and histone methylation in an Epac-dependent manner.
results suggest that PDE4A may be important in the regulation of emotional memory and anxiety-like behavior, but not emesis
This study showed that long PDE4 isoforms provide a novel node for cross-talk between the cAMP and p38 MAPK signalling systems at the level of MK2.
Increased cAMP may remodel cAMP-mediated signalling events by not only increasing the expression of specific PDE4 cAMP phosphodiesterases but also by down-regulating specific isoforms, such as is shown here for PDE4A10 in cardiac myocytes.
a new mechanism in which phosphodiesterase PDE4A4/5 interacts with p75(NTR) to enhance cAMP degradation
In human large intestinal circular muscle, the intracellular pathway of 5-HT4 receptors facilitating cholinergic neurotransmission to large intestinal circular smooth muscle is controlled by phosphodiesterase 4.
PDE4 and Epac1 expression levels are increased in rectal carcinoma tissues, suggesting that the two proteins may be involved in the development of this malignancy. Meanwhile, correlations between PDE4 and Epac1, PDE4 and Cx43, PDE4 and cyclin E1, and Epac1 and Cx43 suggested synergistic effects of these proteins in promoting rectal carcinoma.
phosphorylation of PDE4A5 by MAPKAPK2 enhances PDE4A5 interaction with p75NTR and that this, in turn, serves to attenuate fibrin degradation
lack of AIP hinders the upregulation of PDE4A8 and PDE4A4 protein seen in sporadic somatotrophinomas.
FCPR16 is a novel PDE4 inhibitor with little emetic potential...Our findings indicate that FCPR16 is a promising pre-clinical candidate for the treatment of PD and possibly other oxidative stress-related neuronal diseases.
Here we describe a compound, BC54, that is a selective inhibitor of enzymes from the cAMP-specific PDE4 and PDE7 families. Consistent with the biological effect of other PDE4 and PDE7 inhibitors, BC54 displays potent anti-inflammatory properties and is superior to a combination of rolipram (a PDE4 inhibitor) and BRL50481 (a PDE7A inhibitor) for inducing apoptosis in chronic lymphocytic leukemia (CLL) cells
Repurposing the PDE4 inhibitor roflumilast for treatment of B-cell malignancies is safe, suppresses the oncogenic PI3K/AKT kinases, and may be clinically active
The expression of PDE4A4 and PDE4A8 in normal pituitary, their increased expression in adenomatous pituitary cells where AIP is meant to participate, and the disruption of the PDE4A4-AIP interaction by AIP mutants may play a role in pituitary tumorigenesis.
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.
Low PDE4A expression is associated with sepsis.
Findings demonstrate loss of PDE4 expression in the striato-thalamo-cortical circuit, which is associated with deficits of spatial working memory in patients with Parkinson disease.
A multifunctional docking site on the catalytic unit of PDE4 that is utilized by multiple interaction partners has been identified.
curcumin exerts its in vitro anti-angiogenic and in vivo anti-tumour properties through combined PDE2 and PDE4 inhibition
After 48 h yessotoxin treatment PDE4A-dependent autophagy, as non-apoptotic programmed cell death, is activated.
AKAP 149-PKA-PDE4A complex localization is related with YTX effect in K-562 cell line
Hydroxycarbamide decreases sickle reticulocyte adhesion to resting endothelium by inhibiting endothelial lutheran/basal cell adhesion molecule (Lu/BCAM) through phosphodiesterase 4A activation.
long-acting beta -agonist and PDE4 inhibitor have a synergistic effect in regulating fibroblast tissue repair functions and PGE2 can modulate the effect of beta -agonist and PDE4 inhibitor at least in part through the mechanism of regulating PDE4 expression
The hPDE4 long isoforms are activated by phosphorylation of a serine located in a conserved RRESF motif in a tandem of N-terminal upstream-conserved regions (UCR).
PDE4A and PDE4C work in redundant fashion to mediate the loss of inhibitory PGE2 signaling in lung fibroblasts.
In phosphoinositide 3-kinasegamma-deficient cardiomyocytes, coincident signaling of the major cardiac PDE3 and PDE4 isoforms orchestrates a feedback loop that prevents calcium-dependent ventricular arrhythmia.
The protein encoded by this gene belongs to the cyclic nucleotide phosphodiesterase (PDE) family, and PDE4 subfamily. This PDE hydrolyzes the second messenger, cAMP, which is a regulator and mediator of a number of cellular responses to extracellular signals. Thus, by regulating the cellular concentration of cAMP, this protein plays a key role in many important physiological processes. Alternatively spliced transcript variants encoding different isoforms have been described for this gene.
phosphodiesterase 4A, cAMP-specific
, phosphodiesterase 4A-like
, phosphodiesterase 4A, cAMP-specific (phosphodiesterase E2 dunce homolog, Drosophila)
, cyclic AMP-specific phosphodiesterase FCPDE4A1A
, cyclic AMP-specific phosphodiesterase OCPDE4A1A
, phosphodiesterase 4A, cAMP specific
, cyclic AMP-specific phosphodiesterase CPPDE4A1A
, cAMP-specific 3',5'-cyclic phosphodiesterase 4A
, cAMP-specific phosphodiesterase PDE4A
, cyclic AMP specific phosphodiesterase PDE4A5A
, phosphodiesterase 4A, cAMP-specific (dunce
, phosphodiesterase E2 dunce homolog, Drosophila
, phosphodiesterase isozyme 4
, cyclic AMP-specific phosphodiesterase SSPDE4A1A