Two zebrafish Keap1-paralogs are equally adept at electrophile-sensing but manifest divergent and co-regulatory electrophile-signaling behaviors.

This sesquiterpene hormone likely acted as a morphogenesis-to-differentiation switch in archaic embryos before it evolved its postembryonic function as the status quo regulator of insect metamorphosis.

Structural and functional approaches unambiguously revealed physiologically relevant lateral interactions between FtsZ protofilaments.

Within minutes after an abrupt increase in membrane tension, yeast cells reduce their membrane tension by modulating their rate of endocytosis and exocytosis, and adapt their endocytic actin machinery.

Downregulation of PTBP1 in neurons, but not astrocytes, alleviates motor symptoms in a Parkinson’s disease mouse model by inducing dopaminergic marker expression in striatal neurons and increasing striatal dopamine levels.

The dynamic phosphorylation of autophagy component WIPI2B is critical to maintain autophagosome biogenesis in neurons, and ectopic expression of WIPI2B can restore rates of autophagosome biogenesis in aged neurons.

The role of placental aging and metabolic stress in driving labor onset is demonstrated, with a novel mouse model of preterm labor in which injection of a prolyl hydroxylase inhibitor stabilizes placental hypoxia-inducible factor 1 and significantly shortens gestational length.

In vivo dopamine neuron imaging-based neuroprotective small molecule screen in larval zebrafish and mechanistic investigation using conditional CRISPR knockout and cell-type-specific RNA-seq analysis, coupled with cross-species analyses including human clinical data interrogation, uncover potential disease-modifying therapeutics for Parkinson's disease (PD).

Lineage transformation in lung cancer is dictated by ERK activity and requires permissive chromatin alterations in the context of targeted therapy resistance.

A lack of ADAM10-mediated shedding increases prion protein levels at the plasma membrane and promotes the generation of pathological prion proteins, which accelerates prion disease in mice.