In response to starvation, C. elegans converts a favorable pheromone that induces aggregation to an unfavorable one that induces a stress-resistant larval stage, thereby altering its chemical message without having to synthesize new pheromones de novo.

Acute myeloid leukemia-specific predictive logic models reveal new therapeutic targets involved in cancer resistance mechanisms paving the way for personalized precision medicine.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

DunedinPACE is a novel DNA methylation biomarker of the pace of biological aging for intervention trials and natural experiment studies investigating how the rate of aging may be changed by behavioral or drug therapy, or by environmental modification.

Intermittent fasting orchestrates molecular shifts, yielding cardiovascular improvements, revealing novel cardioprotective mechanisms, and suggesting innovative pharmacological strategies for cardiovascular disease prevention and treatment.

Nuclear magnetic resonance analysis revealed the structural and dynamical changes in MgtE during the channel closure caused by the cooperative Mg²⁺-binding, which had remained undescribed only by a static crystal structure.

Circulating myeloid cells invade the brain during pancreatic cancer, where they accumulate at a unique central nervous system interface and drive anorexia and muscle catabolism.

Genetic analyses using the fruit fly illustrate how neuronal system couples germline stem cell increase to an external cue, which is mating, through stem cell niche signaling.

YTHDC1 is an essential factor controlling satellite cell regenerative ability through multifaceted gene regulatory mechanisms in myoblast cells.

Activation of a DNA-damage cell cycle checkpoint during aging causes genome instability and senescence in yeast mother cells.