Anti-PDE2A3 antibody
Description
Application Data
Description
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An antibody against cGMP-dependent 3′,5′-cyclic nucleotide phosphodiesterase (PDE2A3). PDE2A has dual specificity for the second messengers cAMP and cGMP.
Application Data
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Data Sheet Material Safety Data Sheet (MSDS)Catalogue number crb2005780 Antibody Anti-PDE2A3 antibody Antigen Peptide KLH conjugated synthetic peptide crb1200989 Protein ID UniprotKB - O00408 (Human), Q922S4 (Mouse) Aliases cGMP-dependent 3',5'-cyclic phosphodiesterase, Cyclic GMP-stimulated phosphodiesterase (CGS-PDE; cGSPDE) Cross-Reactivity Human, Mouse Host Species Rabbit Antibody Type Polyclonal Concentration 2.0 mg/ml Glycine Target cGMP-dependent 3',5'-cyclic phosphodiesterase Storage Stabilisers The product should be stored at -20°C for short term storage and long term storage. Avoid repeated freeze/ thaw cycles. Storage The product should be stored at -20°C for short term storage and long term storage. Avoid repeated freeze/ thaw cycles. References Lorigo et al., (2022). PDE-Mediated Cyclic Nucleotide Compartmentation in Vascular Smooth Muscle Cells: From Basic to a Clinical Perspective. J. Cardiovasc. Dev. Dis., 9(1): 4. doi: 10.3390/jcdd9010004.
Sadek et al., (2020). Therapeutic Implications for PDE2 and cGMP/cAMP Mediated Crosstalk in Cardiovascular Diseases. Int. J. Mol. Sci., 21(20): 7462. doi: 10.3390/ijms21207462.
Phosphodiesterases regulate signalling by cyclic nucleotides in diverse processes such as cardiac contractility, platelet aggregation, lipolysis, glycogenolysis, and smooth muscle contraction. There are 3 splice variants of the cGMP-dependent 3′,5′-cyclic phosphodiesterase PDE2A (PDE2A1–PDE2A3), which differ at the N-terminal domain designating their intracellular localization. PDE2A3 localises to distinct membrane fractions. PDE2A3 has dual specificity for the secondary messengers’ cAMP and cGMP.
A new role for PDE2A3 is emerging in the cardiovascular system. Mouse models show that cardiomyocyte PDE2A3 overexpression leads to a lower basal heart rate and protects against arrhythmogenesis from cardiac stress. Also, overexpression protects the mouse model against arrhythmia-induced early death after myocardial infarction.