Flexibility is a defining feature of AKAP kinase-phosphatase assemblies and points toward a mechanism whereby combinatorial recruitment of binding partners tailors the overall conformation of the macromolecular assembly, allowing customized physiological roles.
An unbiased genetic screen in Drosophila provides evidence for a direct link between glial Ca2+ 25 signaling and classical functions of glia in buffering external K+ as a mechanism to regulate neuronal excitability.
TORC2-Ypk1 signaling upregulates flux through the sphingolipid pathway not only by increasing the supply of long-chain base precursors, but also by increasing their use in synthesizing complex sphingolipids.
Global phosphoproteomic analysis in nerve terminal during exocytosis reveals 252 uniquely regulated phosphosites, highlighting complex regulation of active zone proteins at multiple sites and the role of specific kinases/phosphatases.
Fibroblast growth factor induces dephosphorylation and inactivation of the NPR2 guanylyl cyclase, thus decreasing cyclic GMP production in growth plate chondrocytes and contributing to FGF-dependent decreases in bone growth.
High-throughput phenotypic screening followed by unbiased target identification reveals a new molecular glue HQ461 that induces CDK12-DDB1 interaction to promote degradation of Cyclin K via the ubiquitin proteasome system.