Mouse models with specific presynaptic knockout demonstrate that Rim1α is subjected to threonine phosphorylation by a novel EPAC-PKCε module, which is essential to presynaptic transmitter release, required for the induction of presynaptic LTP, and critical for motor learning.

Live cell imaging shows that the cAMP-sensor Epac2, a target of major antidiabetic drugs, is central to fusion pore control during insulin granule exocytosis.

The inhibition of EPAC1, a cAMP-binding protein, appears as a potential therapeutic strategy to limit doxorubicin-induced cardiotoxicity without interfering with its antitumoral activity.

The cAMP sensor and effector Epac2 facilitates dopamine release and promotes cocaine reward.

A new genetically encoded sensor robustly detects exogenously applied PAC1R ligands in vitro, ex vivo, and in vivo (in zebrafishes and mice) serving as a useful resource for probing PAC1R functions.

A novel signaling system in heart mitochondria in which the byproduct of energy metabolism, CO₂/bicarbonate, acts as the primary signal to tune mitochondrial ATP production while keeping energy supply in tight synchronization with energy consumption.

Blocking a protein known as EPAC1 may prevent the development of heart-related side effects caused by a chemotherapy drug.

Placing the PACAP/PAC1 signaling within glutamate/GABA cell type and subregional contexts in mouse brain reveals its conspicuous role for sensorimotor circuit interaction through modulating neuronal plasticity.

cAMP is identified to play a novel role in regulating DNA demethylation and gene transcription by augmenting the intracellular reactive Fe(II) pool.

ePAC, a novel cancer vaccine utilizing a mammalian-derived virus-like particle to co-deliver neoantigens and CpG-ODN, demonstrates strong antitumor efficacy in mouse models.