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Decay rate of mRNAs encoding inflammatory regulators is controlled by the balance between AU-rich element-mediated deadenylation and cytoplasmic polyadenylation element-mediated polyadenylation.

Biochemical approaches and cellular experiments show a novel effect of METTL3 on homologous recombination repair and chemotherapeutic response via the m6A-YTHDC1-dependent regulation of the EGF/RAD51 axis.

Whether deforming cells behave as elastic balls (deforming at constant volume) or as sponges (loosing volume as they deform) depends on how fast they change their shape, because the cell volume depends on the tension of the plasma membrane.

A high-resolution approach for monitoring dry mass and the density of that dry mass on a single-cell level is developed and used to reveal that mammalian cells can lose components in mitosis due to lysosomal exocytosis.

Activity-dependent bidirectional changes in phosphorylation of the autism-associated scaffold protein Shank3 are essential for the expression of homeostatic synaptic plasticity.

MDGAs are highly diffusive molecules that alter both neuroligin-1 and AMPA receptor dynamics and function, thereby significantly delaying the differentiation of excitatory post-synapses.

Wild-type human recombinant tau protein infused in presynaptic terminals newly assembled microtubules, which sequestered cytosolic dynamins, thereby blocking synaptic vesicle endocytosis and causing activity-dependent rundown of excitatory synaptic transmission in a slice model of mouse brainstem.

This first evidence of oligogenic inheritance in failed spermatogenesis strongly suggests that oligogenic heterozygosity could explain a significant proportion of asthenoteratozoospermia cases.

Gene regulation by C/EBPβ determines how surplus of dietary fat is stored, which has consequences for metabolic health.

In a chemical genetics study, JM03 derived from crotamiton, an inhibitor of trainsient receptor potential vanilloid-4 channels, was identified to extend lifespan and improve oxidative and hypertonic stress resistance in Caenorhabditis elegans via inhibiting OSM-9.