A genetic basis underlying cell resilience against metabolic stress in cells of a hibernator, Arctic ground squirrels, has been discovered.

Biochemical and microscopy-based approaches in mouse and human macrophages reveal that glycine cytoprotection acts at the level of the newly identified pan-death protein NINJ1 to inhibit multiple lytic cell death pathways, thereby resolving a long-standing mechanism of glycine cytoprotection.

Candida albicans cells respond in two distinct ways to fluconazole exposure where cells enter the Ribo-dominant state characterized by an upregulation of ribosomal-related proteins and processes, or cells enter the Stress-dominant state characterized by the upregulation of stress responses.

Oxidative stress leads to the translocation of Rab5 from endosome to mitochondria, regulated by ALS/Alsin, a component associated with amyotrophic lateral sclerosis, leading to mitochondrial-endosomal physical contacts and a cytoprotective response.

Cdk5-mediated stabilization of Acinus in postmitotic neurons promotes autophagy and the removal of protein aggregates linked to neurodegeneration in Drosophila melanogaster.

Biochemical and biological studies reveal that caspases feed back onto the Unfolded Protein Response by cleaving the ER-stress sensor IRE1 to produce a cytoprotective N-terminal fragment that inhibits BAX-dependent apoptosis.

Oligodendrocytes with an enhanced ability to withstand cytotoxic stress display an increased capacity to remyelinate demyelination lesions of the CNS in the presence of an inflammatory environment.

IL4i1 is an amino acid oxidase expressed in the mammalian immune system and snake venoms, which control diametrically opposite cell protection versus cell death pathways, respectively.

Ceapins enable selective pharmacological inhibition of the cytoprotective transcriptional response to endoplasmic reticulum stress through ATF6α without affecting other branches of the unfolded protein response.

Characterization of PML subnuclear structures during human cytomegalovirus infection demonstrates that prolonged interferon and DNA damage signaling can induce giant PML nuclear bodies which sequentially entrap both nucleic acids and viral proteins as a cytoprotective mechanism.