Judith Hüttemeister, Franziska Rudolph ... Michael Gotthardt
Titin’s regulated integration and mobility after cell fusion support syncytium formation in culture, while limited diffusion in vivo highlights a key challenge for developing effective cell-based therapies for skeletal muscle diseases.
Cytoskeleton rearrangements promote formation of a giant structure called a GUVac that stops cells from dying when they become detached from the extracellular matrix.
In astrocytes, there exists an intrinsic spatial threshold of subcellular calcium levels that triggers an astrocyte calcium surge throughout the cell, demonstrating cellular astrocyte calcium integration of time and space.
Neurodegeneration driven by pathogenic aggregating proteins reorganizes the actin cytoskeleton, causing cellular stiffening and abolishing force generation required for endocytic events.
The viscous hydraulics of contracting endoplasmic reticulum networks challenge common solute transport theories, suggesting the contraction of peripheral sheets as a plausible driving mechanism.
