cAMP
- A non-catalytic function of PI3Kγ drives smooth muscle cell proliferation after arterial damage
Highlighted Article: PI3Kγ regulates VSMC proliferation independently of its kinase activity by controlling cAMP levels through PDE4D.
- Mitochondrial cAMP exerts positive feedback on mitochondrial Ca2+ uptake via the recruitment of Epac1
Highlighted Article: The Ca2+-dependent formation of mitochondrial cAMP by matrix-localized soluble adenylyl cyclase intensifies further Ca2+ uptake into the organelle; this convergence of signalling pathways supports steroidogenesis.
- EPAC1 activation by cAMP stabilizes CFTR at the membrane by promoting its interaction with NHERF1
Summary: Activation of the cAMP sensor EPAC1 leads to stabilization of CFTR at the plasma membrane, through a mechanism that involves the PDZ adaptor NHERF1, and could be used to increase the rescue of mutant CFTR.
- Correctors of mutant CFTR enhance subcortical cAMP–PKA signaling through modulating ezrin phosphorylation and cytoskeleton organization
Highlighted Article: Correctors of F508del CFTR, by activating ezrin and actin cytoskeleton re-organization, generate a sub-cortical pool of cAMP of adequate amplitude to activate chloride secretion.