Recombinant human PDE3B protein

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

PDE3B also known as cGMP-inhibited phosphodiesterase B is an enzyme with a role in cyclic nucleotide signaling. It possesses a molecular mass of approximately 133 kDa. PDE3B predominantly gets expressed in adipose tissue liver and to some extent in the heart. It breaks down cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) which play key roles in cellular signaling. By hydrolyzing these cyclic nucleotides into their non-cyclic forms PDE3B regulates intracellular levels of these molecules.

Biological function summary

In adipose tissue and liver PDE3B modulates lipogenesis and lipolysis which are vital processes for energy balance. This enzyme interacts with signaling pathways that involve protein kinase A (PKA) and insulin signaling. PDE3B operates as part of larger protein complexes and influences the metabolic rate by regulating the availability of the cAMP for phosphorylation reactions. The activity of PDE3B links closely to the control of energy homeostasis due to its regulatory function on lipid metabolism.

Pathways

PDE3B is integral to the insulin signaling pathway and adiponectin signaling pathway both important in glucose and lipid homeostasis. Within these pathways it functions alongside proteins like AKT and PKA where its activity modulates their signaling efficiency. By controlling the balance of cAMP PDE3B influences signaling cascades that are important for the adaptive cellular responses to hormones and nutrients.

PDE3B connects to conditions such as obesity and type 2 diabetes due to its involvement in energy homeostasis and lipid metabolism. In type 2 diabetes the dysregulation of PDE3B activity affects insulin signaling and glucose uptake. Additionally in the context of obesity PDE3B activity shifts the balance of lipolysis and lipogenesis influencing adipose tissue mass and function. Proteins such as insulin receptors and PKA become closely tied to PDE3B in these disorders highlighting its role in metabolic disease mechanisms.