A Syt1-tdTomato transgenic mice with normal synaptic transmission is established to label synapse in situ and screen synaptogenic adhesion molecules.

Molecular genetic, cell culture as well as electrophysiological analyses reveal a C1ql2/Neurexin3(25b+)-dependent molecular pathway through which Bcl11b controls critical functions of adult hippocampal mossy fiber synapses.

ORAI1 ion channel lipid modification is required for a proper immune synapse formation and T cell activation.

A novel Aβ-driven inhibitory mechanism on γ-secretases, which leads to substrate accumulation and reduced release of products, contributes to neurotoxicity by impairing γ-secretase signaling and might operate in Alzheimer’s disease.

An agonist antibody to MuSK, delivered after disease onset, decreases the loss of neuromuscular synapses, improves motor function and extends the lifespan of ALS mice.

Specific inhibition of cyclin-dependent kinase-like 5 (CDKL5), a kinase linked to a severe neurodevelopmental disorder, demonstrates an important role in the regulation of excitatory hippocampal synapses and synaptic plasticity that was not previously appreciated in rodent knock-out models.

Protein kinase A regulates the rapid, activity-dependent genesis of excitatory synapses during striatal development.

Inducible degradation of the insulin/insulin-like growth factor-1 receptor shows that a doubling in lifespan is possible even at extremely old ages in an organism.

Arp2/3 complex-mediated actin polymerization shapes how B lymphocytes probe the surface of antigen-presenting cells, promotes coalescence of B cell receptor (BCR) microclusters, amplifies BCR signaling, and enhances B cell activation.

A combination of electrophysiological, electrochemical, and anatomical experiments sheds new light on how the complex neurotransmitter repertoire of dopaminergic neurons in the brain is regulated by proteins of the neurexin family.