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Biomolecular condensates, which form via liquid−liquid phase separation in a tightly regulated manner, have fundamental roles in cellular organization and physiology. Recent studies provide insight into how cellular stress, ageing-related loss of homeostasis and a decline in protein quality control may contribute to the formation of aberrant, disease-causing condensates.
p38α — the best-characterized member of the p38 kinase family — is a key mediator of cellular stress responses. p38α is activated by a plethora of signals and functions through a multitude of substrates to regulate different cellular behaviours. Understanding context-dependent p38α signalling provides important insights into p38α roles in physiology and pathology.
Ferroptosis is a form of regulated cell death driven by iron-dependent phospholipid peroxidation. Since its formal identification in 2012, multiple studies have addressed molecular mechanisms, regulation and functions of ferroptosis, associating this cell death modality with various pathologies, but also proposing its roles in normal physiology and potential for therapeutic targeting.
Tissue morphogenesis is instructed by the interplay of biochemical cues, mechanics and tissue geometry. Conceptually, these instructions can be deployed either deterministically, functioning as a pre-patterned programme for shape changes, or stochastically, whereby the shape emerges in a self-organized fashion. This Review discusses recent insights into how pre-patterned and stochastic tissue shaping are integrated during development.
Insulin secretion from pancreatic β-cells is potently activated by an increase in glucose after feeding but other dietary components — amino acids, fatty acids, metabolites, α-cell-produced peptides and gastrointestinal tract hormones — further control this response. Deciphering this complex regulation is important to increase our understanding of pancreatic dysfunction in diabetes.