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Literature summary for 3.1.4.17 extracted from

  • Baliga, R.S.; Preedy, M.E.J.; Dukinfield, M.S.; Chu, S.M.; Aubdool, A.A.; Bubb, K.J.; Moyes, A.J.; Tones, M.A.; Hobbs, A.J.
    Phosphodiesterase 2 inhibition preferentially promotes NO/guanylyl cyclase/cGMP signaling to reverse the development of heart failure (2018), Proc. Natl. Acad. Sci. USA, 115, E7428-E7437 .
    View publication on PubMedView publication on EuropePMC

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
3',5'-cGMP + H2O Mus musculus
-
5'-GMP
-
?

Organism

Organism UniProt Comment Textmining
Mus musculus Q922S4
-
-

Source Tissue

Source Tissue Comment Organism Textmining
cardiomyocyte cell line
-
Mus musculus
-
heart
-
Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3',5'-cGMP + H2O
-
Mus musculus 5'-GMP
-
?

Synonyms

Synonyms Comment Organism
PDE2A
-
Mus musculus
phosphodiesterase 2
-
Mus musculus

General Information

General Information Comment Organism
malfunction blockade of isoform PDE2 promotes cGMP signaling to offset the pathogenesis of experimental heart failure (induced by pressure overload or sympathetic hyperactivation), reversing the development of left ventricular hypertrophy, compromised contractility, and cardiac fibrosis Mus musculus