A phase transition of TIR-1/SARM1 induced by either pathogen or non-pathogen stress potentiates its intrinsic NADase activity, which activates the p38 PMK-1 signaling cascade to induce protective immune defenses in Caenorhabditis elegans intestinal epithelial cells.

The subcellular localization of the prolyl hydroxylase oxygen sensor in C. elegans neurons is regulated by p38 MAP kinase signaling.

The p38 MAPK pathway functions downstream of a cell-size-sensing process to coordinate cell size/growth with G1 progression in animal cells.

Axon degeneration due to loss of mitochondria is suppressed by CaMKII activity and MAP kinase signaling.

Lack of cardiac MKK6 results in premature death with the development of heart hypertrophy and cardiac dysfunction in aging.

Src, an oncogene, promotes both cell proliferation and cell death simultaneously, which can be regulated by dietary methionine.

A link between chronic stress and organ dysfunction is explained by the gateway reflex, in which brain micro-inflammation at specific vessels establishes a new neural pathway to induce fatal organ failure particularly in gastrointestine and heart.

The amount of secreted Pgk1 is sharply decreased in Rtn4al/NogoA-overexpressed muscle cells, leading to various manifestations of neurodegenerative disease, including denervated neuromuscular junction and failed neurite outgrowth of motoneurons.

Various types of stress reset heritable small RNA responses through the function of the p38 MAPK pathway, the transcription factor SKN-1/Nrf2, and the MET-2/SETDB1 putative histone methyltransferase.