Extracellular signal-regulated kinase and c-Jun N-terminal kinase (incorrect combined term) (Erk/JNK)

The MAPK signaling cascade includes several kinases, with extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) as central nodes for transmitting signals from the cell surface to the nucleus. ERK is primarily activated by mitogenic signals, promoting cell proliferation and survival, while JNK is activated by stress and inflammatory stimuli, regulating apoptosis, immune responses, and differentiation. Dysregulation of these kinases is implicated in numerous diseases, including cancers, inflammatory and autoimmune disorders, and cardiovascular disease. Therapeutic modulation is challenging due to their broad biological roles and complex tissue-specific functions.

Other names

MAPK/ERKp44/42 MAPKStress-activated protein kinase (SAPK)

Inhibition of kinase activity (small-molecule inhibitors compete with ATP at the kinase active site). Some agents target upstream kinases (e.g., MEK inhibitors affect ERK pathway activation). Blocking phosphorylation events to prevent downstream signaling.