Johannes Wilhelm Hell

This study shows that S-nitrosylation of PKA regulatory subunits by SCAN is required for GPCR-induced PKA activation in heart, brain, and fat tissues.

This paper identifies a mechanism by which amyloid beta potentiates CaV1.2 channels via β2AR, leading to synaptic dysfunction and neurotoxicity, and shows that disrupting this pathway prevents these effects.

This study identifies the α1 adrenergic receptor - PKC - Pyk2 - Src signaling pathway as a mechanism boosting CaV1.2 channel activity and LTP in rodents.

Buonarati et al. show that β-adrenergic stimulation enables LTP induction in response to LTD stimuli by switching synaptic CaMKII movement to LTP mode.

The paper shows that Alpha-Actinin-1 enhances CaV1.2 channel activity by localizing it to specific sites and increasing its open probability.