Specifications
Immunogen
Synthetic peptide corresponding to amino acids in C-terminal of Human PDE 10A, common to the 10A enzyme.
Applications
Application Notes
WB: 1/2000.
Target
Alternative Names
PDE10A; phosphodiesterase 10A; cAMP and cAMP-inhibited cGMP 3,5-cyclic phosphodiesterase 10A; phosphodiesterase 10A1 (PDE10A1); dJ416F21.1 (phosphodiesterase 10A); HSPDE10A; FLJ11894; FLJ25677;
Product Background
Antigen Description
Plays a role in signal transduction by regulating the intracellular concentration of cyclic nucleotides. Can hydrolyze both cAMP and cGMP, but has higher affinity for cAMP and is more efficient with cAMP as substrate.
Pathway
G alpha (s) signalling events; GPCR downstream signaling; Hemostasis; Morphine addiction; Nitric oxide stimulates guanylate cyclase; Platelet homeostasis;
Citations
Publication ()
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Molecular unbalances between striosome and matrix compartments characterize the pathogenesis of Huntington’s disease model mouse
Morigaki R, Yoshida T, Fujikawa J, Crittenden JR, Graybiel AM
Applications: IHC
Reactive species: Human
"Abstract: The pathogenesis and pathophysiology of Huntington's disease (HD) are still incompletely understood, despite the remarkable advances in identifying the molecular effects of the Htt mutation in this disease. Clinical positron emission tomography studies suggest that phosphodiesterase 10A (PDE10A) declines earlier than dopamine D1 and D2 receptors in HD, indicating that it might serve as a key molecular marker in understanding disease mechanisms. In movement disorders, mutations in the genes encoding PDE10A and G-protein α subunit (Gαolf), both critical cAMP regulators in striatal spiny projection neurons, have been linked to chorea and dystonia. These observations highlight the potential importance of striatal cyclic AMP (cAMP) signaling in these disorders, but how such dysfunction could come is unknown. Here, we suggest that a key to understanding signaling dysfunction might be to evaluate these messenger systems in light of the circuit-level compartmental organization of the caudoputamen, in which there is particular vulnerability of the striosome compartment in HD. We developed machine learning algorithms to define with high precision and reproducibility the borders of striosomes in the brains of Q175 knock-in (Q175KI) HD mice from 3-12 months of age. We demonstrate that the expression of multiple molecules, including Gαolf, PDE10A, dopamine D1 and D2 receptors, and adenosine A2A receptors, is significantly reduced in the striosomes of Q175KI mice as compared to wildtype controls, across 3, 6, and 12 months of age. By contrast, mu-opioid receptor (MOR1) expression is uniquely upregulated, suggesting a compartment-specific and age-dependent shift in molecular profiles in the Q175KI HD mouse model caudoputamen. These differential changes may serve as a useful platform to determine factors underlying the greater vulnerability of striatal projection neurons in the striosomes than in the matrix in HD."
Article snippet: The immunizing peptide-blocking assay for rabbit polyclonal PDE10A (Creative Diagnostics, Shirley, NY, USA) was performed as described previously. 
Figure 1. Positive control showing PDE10A immunostaining using an anti-PDE10A antibody.
COA
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