To promote longevity under heat stress shares yeast aging factors with progeny through a down-regulation of the diffusion barrier in the membranes between the mitotic cells.

Differential eIF4E binding to transcription initiation nucleotides and alternative promoter usage of eIF1A, PABP and other genes are involved in the response of the translation machinery to energy stress.

Endoplasmic reticulum stress in yeast activates not only the UPR but also Rpn4, promoting the clearance of misfolded proteins from the cytosol as part of a modular cross-compartment stress response.

Arabidopsis deploys the core signalling module that perceives distinct stress signals, such as DNA damage and heat stresses, and represses G2/M-specific genes, thereby causing cell cycle arrest.

The orphan receptor GPR158 is highly regulated by stress exposure and acts on key neuronal signaling pathways in the prefrontal cortex to control depressive-like behaviors.

ATF4, the master regulator of transcription during the Integrated Stress Response (ISR), causes global changes in cysteine sulfhydration of proteins and this event causes cellular metabolic reprogramming.

The well-established link between stress and depression could be due to the activity of a population of cells in prefrontal cortex that express a gene mutated in the rare disorder Wolfram syndrome.

A drug-like molecule called ISRIB, which activates the translation initiation factor eIF2B, antagonizes stress responses as diverse as protein misfolding and nutrient deprivation, and restores protein synthesis, enhancing memory.

LRH-1/NR5A2 responds to ER stress by inducing a novel pathway that is required for stress resolution in mice and can be targeted by LRH-1 agonists.

MARCH5 mediates a pathway driving MCL1 degradation in response to cellular stress, which sensitizes to BH3 mimetic drugs targeting BCLXL and provides a broadly effective therapeutic strategy for solid tumors.