Extracellular signal-regulated kinase and c-Jun N-terminal kinase pathway components (ERK and JNK pathway components)

The Extracellular Signal-Regulated Kinase (ERK) and c-Jun N-terminal Kinase (JNK) pathway components are essential elements of the mitogen-activated protein kinase (MAPK) signaling network, which coordinates cellular responses to a variety of stimuli. The ERK pathway, specifically the Raf-MEK-ERK cascade, is primarily triggered by growth factors and is a fundamental driver of cell proliferation, differentiation, and survival [1]. Mutations in upstream components like RAS and BRAF frequently lead to constitutive ERK activation, a common feature in many human malignancies [4]. In contrast, the JNK pathway is a key component of the stress-activated protein kinase (SAPK) group, responding to environmental stressors and pro-inflammatory cytokines to regulate apoptosis and inflammation [2]. While MEK and ERK inhibitors are established therapies in oncology, JNK inhibitors are being explored for their potential in treating inflammatory and neurodegenerative conditions [3]. However, the clinical utility of targeting these pathways is often limited by complex feedback mechanisms, pathway crosstalk, and significant systemic toxicities such as dermatologic and gastrointestinal issues [4]. Sources: [1] Guo, Y. J., et al. (2020). "The MAPK/ERK signaling pathway: Molecular mechanism and therapeutic targets in cancer." Signal Transduction and Targeted Therapy. [2] Bubici, C., & Papa, S. (2014). "JNK signalling in cancer: in need of new, smarter therapeutic targets." British Journal of Cancer. [3] Mehan, S., et al. (2011). "The role of JNK signaling in neurodegenerative diseases." Journal of Alzheimer's Disease. [4] Caunt, C. J., et al. (2015). "MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road." Nature Reviews Cancer.

Other names

MAPK pathway componentsERK/JNK signaling cascadeStress-activated protein kinase pathwayMitogen-activated protein kinase pathway

Inhibition of the kinase activity of specific components within the MAPK cascade, such as MEK1/2, ERK1/2, or JNK1/2/3, thereby preventing the phosphorylation of downstream substrates and modulating gene expression.