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Electrophysiological and optical analysis of neurotransmitter release at central synapses reveals that glutamate signalling is not required for the long-term potentiation (LTP) of presynaptic function, and instead only promotes presynaptic long-term depression (LTD).

In vivo and in vitro elongation factor-RNA interaction data provide a missing link in understanding how processive elongation complexes are formed on active genes and disassembled at the end of genes.

OptoGranules reveal the function of G3BP1 as a stress granule scaffold and demonstrate that protracted stress granule assembly is sufficient to drive neurodegeneration and the evolution of ALS-FTD pathology.

Biochemically detailed modelling of pathways leading to post-synaptic plasticity reveals the dependence of neocortical LTP/LTD on the availability of different proteins and stimulation patterns.

Idiopathic patients along a complex motor neuron disease-dementia spectrum exhibit mRNA splicing changes that are due to multi-protein insolubility.

There are at least two separate pathways for AMPA receptor recycling, which are regulated by synaptic activity.

Three distinct AKT isoforms are found in the brain and show dissimilar patterns of expression, differential roles in the expression of synaptic plasticity, and different roles in neuronal signaling.

Acute myeloid leukemia-specific predictive logic models reveal new therapeutic targets involved in cancer resistance mechanisms paving the way for personalized precision medicine.

Computational models of large-scale cortical dynamics, integrating gene expression mapping to pattern pharmacological modulation across cortex, capture inter-areal topographies of functional connectivity alterations induced by lysergic acid diethylamide, providing a framework for simulating effects of pharmacology in the human brain.

ERK activation during induction of long-term synaptic plasticity is enhanced by synergistic interactions among signaling pathways mediated by the synaptically located GTPase-activating protein, and each pathway contributes to different ERK temporal dynamics.