Mitogen-activated protein kinase kinase (MEK) and extracellular signal-regulated kinase (ERK) pathway components (MEK/ERK pathway (component abbreviations include MEK, ERK))

Mitogen-activated protein kinase kinase (MEK) and extracellular signal-regulated kinases (ERK) are core enzymes in the highly conserved MAPK/ERK signaling pathway. This pathway transduces signals from cell-surface receptors such as receptor tyrosine kinases to the nucleus, orchestrating critical cellular programs including proliferation, differentiation, and survival. The core architecture involves activation of RAS (a small GTPase), which thereby activates the RAF kinase, leading to phosphorylation and activation of MEK1/2 (MAP2K1/2), which then phosphorylate ERK1/2 (MAPK3/1). Activated ERK enters the nucleus to phosphorylate a wide array of transcription factors. Deregulation of this cascade is well established in various cancers, particularly through mutations in upstream components like RAS and BRAF, making the pathway a principal focus for targeted cancer therapies. Approved drugs primarily target MEK and to a lesser extent ERK, but resistance remains a clinical challenge due to redundancy and feedback within the broader network of cellular signaling pathways[1][4][5][6][7][8].\n\nPlease note that while \"Mitogen activated protein kinase kinase/extracellular signal-regulated kinases pathway components\" refers collectively to critical signaling molecules, for unambiguous scientific or clinical contexts it is essential to specify individual kinases (e.g., MEK1, ERK2) or refer to the \"MAPK/ERK signaling pathway\" as a general mechanism, but not as a discrete single-molecule drug target[7][3][4].

Other names

MEK/ERK pathwayMAPK/ERK pathwayRAS-RAF-MEK-ERK pathwayMitogen-activated protein kinase pathwayMAPK cascade

Inhibition of kinase activity (ATP-competitive or allosteric inhibition of MEK or ERK)\nSuppression of downstream phosphorylation events and gene transcription\nIndirect tumor suppression by blocking proliferation or promoting apoptosis