Browse our latest research

A combination of electrophysiological, immunocytochemical, and biochemical approaches elucidate the mechanisms by which the transcriptional regulator REST/NRSF rescues neuronal homeostasis by upregulating GABAergic transmission selectively onto excitatory neurons in response to hyperactivity.

The IRE1/XBP1 signaling in myofibers is essential for robust skeletal muscle regeneration in response to injury.

A peroxidase-containing nanocompartment in the bacterial pathogen Mycobacterium tuberculosis protects against oxidative stress and antibiotic treatment in the host.

The motor-relevant properties of the myriad objects with which we interact on a daily basis are encoded in memory using categorical representations, or 'object families'.

Through interactions with both ubiquitin units that emanate from a branch point in polyubiquitin, UCH37 recognizes and hydrolyzes branched chains to promote proteasome-mediated degradation upon proteolytic stresses.

Computational models of gating processes in an ion channel show how stability shifts upon ligand-binding and mutations are reproduced, which highlights mechanistic details and proposes a new role for symmetry in gating.

Ca²⁺-dependent nuclear entry of Ca²⁺/calmodulin-dependent protein kinase-1 in sensory neurons, taking place with a relatively slow kinetics, contributes to couple long-lasting sensory stimulations with signaling in the nucleus over a timescale relevant for sensory history-dependent plasticity.

By fusing influenza viral conserved epitopes and a superantigen fragment, we constructed a recombinant protein that might be a candidate universal broad-spectrum vaccine for the prevention and treatment of multiple influenza viruses.

In the dioecious plant genus Leucadendron, shifts to sex-biased gene expression occurred predominantly in genes with ancestrally high rates of expression evolution, and were not correlated with morphology.

Functional characterization of the alpha/B1.1.7 SARS-CoV-2 variant revealed an eightfold affinity increase of the N501Y RBD to human ACE-2 and that even a low inoculation dose of the alpha variant induces severe disease and fast progression in transgenic hACE2 mice.