Low-level features of peripheral saccade targets are fed back to early foveal retinotopic cortex in a signal that resembles activation elicited by direct foveal presentation.
Genetic and electrophysiological studies uncover a mechanism linking a TTN missense variant to atrial fibrillation by coupling titin with potassium channel remodeling, revealing FHL2 as a modulator and therapeutic target.
Clinically relevant Ω-loop mutations in PDC-3 reshape active-site dynamics to enhance β-lactamase activity, providing mechanistic insights that can guide the rational design of inhibitors.
