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Loss of BAF47 destabilizes the BAF complex on chromatin, and reintroduction of BAF47 leads to enhancer activation and Polycomb opposition at bivalent promoters. BAF47 loss affects BAF and PBAF complexes, which have distinct functions in regulation of enhancers and promoters.
The precise underpinnings of Parkinson's disease and other disorders associated with the accumulation of α-synuclein are unclear. This study shows that PrPC mediates α-synuclein-associated synaptic dysfunction and memory deficits. Blocking specific events in receptor biology rescued cognitive deficits in mice, suggesting new possibilities for intervention in synucleinopathies.
Wu et al. show that prosurvival BCL-2 proteins disrupt SUFU repression of GLI activity, leading to GLI target gene expression. BH3 mimetics disable GLI transcriptional activity driven by HH pathway mutations.
Emerging data indicate that exercise modulates cancer biology and disease outcomes; however, the molecular mechanisms are poorly established. In this Opinion article, the authors speculate on how exercise might reprogramme the tumour microenvironment to influence cancer hallmarks.
Using DNA barcoding, Lan et al. investigated the clonal evolution and dynamics of glioblastoma cells, and propose a model whereby proliferative heterogeneity is derived from stochastic fate decisions made by a homogeneous population of glioblastoma stem cells and their progeny.
Thiazide diuretics lower blood pressure and cardiovascular risk but can cause severe hyponatraemia. Researchers now demonstrate that thiazide-induced hyponatraemia is associated with a genetic variant in a distal nephron prostaglandin transporter. They propose that reduced prostaglandin reabsorption through this transporter facilitates activation of the prostaglandin EP4 receptor to increase water reabsorption.