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Human PDE4A Protein expressed in HEK-293 Cells - ABIN2728507
Taniguchi, Iizumi, Watanabe, Masuda, Morita, Aono, Toriyama, Oishi, Goi, Sakai: Resveratrol directly targets DDX5 resulting in suppression of the mTORC1 pathway in prostate cancer. dans Cell death & disease 2016
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
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.
Data demonstrate that upregulation of Nox4 leads to an upregulation of PDE4A, B, and D and increased hydrolysis of cAMP which in turn augments cell replication and angiogenesis.
These results indicate that PDE4A and PLAT may be susceptibility genes for schizophrenia in the Japanese population.
we have identified a so-far-unknown interaction between LIS1 and PDE4 isoforms, whereby PDE4 can modulate LIS1-dynein complexes and dynein-dependent processes within cells by sequestering LIS1.
PDE4 expression is reduced in failing human heart. PDE4 affects local but not global cAMP levels in human cardiomyocytes.
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