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AKT1 — PDE3B

Pathways - manually collected, often from reviews:

• KEGG Insulin signaling pathway: AKT1/AKT2/AKT3 → PDE3A/PDE3B (protein-protein, activation)
• KEGG Progesterone-mediated oocyte maturation: AKT1/AKT2/AKT3 → PDE3A/PDE3B (protein-protein, activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: AKT1 — PDE3B (in vivo) Kitamura et al., Mol Cell Biol 1999*
• IRef Hprd Interaction: AKT1 — PDE3B (in vitro) Kitamura et al., Mol Cell Biol 1999*

Text-mined interactions from Literome

Kitamura et al., Mol Cell Biol 1999 : Insulin induced phosphorylation and activation of endogenous or recombinant PDE3B in 3T3-L1 adipocytes have now been shown to be inhibited by a dominant negative mutant of the serine-threonine kinase Akt, suggesting that Akt is necessary for insulin induced phosphorylation and activation of PDE3B ... These results suggest that PDE3B is a physiological substrate of Akt and that Akt mediated phosphorylation of PDE3B on serine-273 is important for insulin induced activation of PDE3B
Zmuda-Trzebiatowska et al., Cell Signal 2007 : Thus, we found that overexpression of PKB induced lipogenesis in a PDE3B dependent manner
Berggreen et al., Am J Physiol Endocrinol Metab 2009 : PKB activity was required for the insulin induced activation of phosphodiesterase 3B (PDE3B) and for the antilipolytic action of insulin ... In summary, we propose that PKB is required for the positive effects of insulin on lipid storage and that regulation of PDE3B and AMPK by PKB is important for these effects