Browse our Research Articles

OCIAD1 associates with prohibitin assemblies and regulates the proteolytic processing and stability of the catalytical Complex III subunit cytochrome c₁.

A multiverse approach consisting of 270 analyses on five independent studies fails to replicate the most common electrophysiological indicator of depression, which is asymmetry of alpha power in frontal regions.

Phasic microfilament behaviors of the growth and stabilization of cortical actin caps are driven by distinct combinations of actin regulatory proteins, which display features of a deep competition for G-actin.

Cross-species transcriptomic analysis and high-throughput behavioral assays in a Drosophila model of Huntington's disease show that downregulation of glial genes involved in synaptic function compensates for disease-related excitotoxicity.

Detailed analysis of transporter expression and glucose uptake rates shows that carbohydrate import at the blood–brain barrier is adapted via TGF-βsignaling-dependent transcriptional regulation of carbohydrate transporters to protect the brain form effects of nutrient shortage.

The first-in-class cell-permeant fluorescent probe provides direct and visual evidence of SARM1 activation in axonal degeneration and identified the first covalent, allosteric inhibitor of SARM1 acting on the NAD-binding pocket in the ARM domain.

Sensory activity within the superior colliculus is read out by downstream motor structures and contributes to individual saccade kinematics with single spike precision.

Adaptation along multiple task-axes reveals choice traces at millisecond resolution in non-invasive recordings from human premotor cortex and provides evidence that theories of top-down control hold even after extensive experience.

The C terminal fusion partners of TAZ-CAMTA1, YAP-TFE3 and potentially other TAZ/YAP fusion proteins in cancer recruit epigenetic modifiers that modulate a baseline TEAD-based transcriptional program.

In models reconstructed from MRI scans of patients with embolic stroke of undetermined source, computational simulations reveal that fibrosis has the intrinsic capacity to sustain arrhythmia drivers when subjected to triggered activity known to exist in patients with atrial fibrillation.