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Formation of a phase-separated interface between homologous chromosomes during meiosis enables regulatory signals to spread in cis over long distances, illuminating the longstanding mystery of crossover interference.

Endoplasmic reticulum (ER) inheritance regulation during ER stress controls the transmission of misfolded ER proteins from mother to daughter cell in budding yeast.

A decline in iron-recycling functions of the splenic red pulp macrophages early during aging is driven by iron loading and involves their damage and a loss in red blood cell clearance capacity.

Heparan sulfate-RAGE interaction is essential for normal function of RAGE in osteoclastogenesis and drug-induced liver damage, which can be targeted to curb RAGE activation as a new opportunity.

Vps29 promotes retromer localization in the adult Drosophila brain, engaging Rab7 and TBC1D5, and its loss triggers age-dependent neuronal impairments in endolysosomal trafficking and synaptic transmission.

Switches in cell state downstream of pathogen exposure are driven by a deeply conserved disorder-to-order phase transition in an immunity signaling network.

Structures of the death domain of the p75 neurotrophin receptor in complex with downstream effectors show how competitive protein-protein interactions orchestrate the hierarchical activation of downstream pathways in non-catalytic receptors.

Analysis of proteomic data identified protein biomarkers of aging, mortality and aging-related diseases, supporting their use to monitor aging trajectories and identify individuals at higher risk of disease.

Loss of function of membrane-bound O-acyltransferase 7 (MBOAT7), but not transmembrane channel-like 4 (TMC4), promotes hepatic steatosis.

Hyperphosphatemia, by itself and in the context of chronic kidney disease, contributes to iron restrictive anemia by directly targeting the liver and elevating proinflammatory cytokines and hepcidin, which contributes to widespread tissue injury, such as skeletal muscle wasting.