Mitogen-activated protein kinase kinase–extracellular signal-regulated kinase signaling pathway (MEK–ERK pathway)

The **MEK–ERK signaling pathway** (also called the MAPK/ERK pathway or Ras–Raf–MEK–ERK pathway) is a canonical intracellular signaling cascade critical for communication from growth factor and cytokine receptors at the cell membrane to transcriptional regulators in the nucleus. The pathway sequence involves activation of receptor tyrosine kinases triggering Ras activation, which then activates Raf kinases, followed by MEK1/2 (MAPK/ERK kinases), which in turn phosphorylate and activate ERK1/2 (extracellular signal-regulated kinases)[1][2][3][5]. ERK1/2 phosphorylate multiple cytoplasmic and nuclear targets, affecting cell proliferation, survival, differentiation, and apoptosis[1][3][5]. Dysregulation of this pathway by activating mutations or amplifications is a central driver in many human cancers, and targeting MEK and ERK has yielded several approved inhibitors for malignancies such as melanoma and being pursued for other indications (e.g., prostate, hepatocellular, colorectal cancers)[2][4][6]. However, the signaling "pathway" is a network, not a single molecule or protein, and is thus broader than most standard drug targets. It is considered druggable, but with challenges due to feedback mechanisms and adaptive resistance[2][6]. Note: - The "MEK–ERK signaling pathway" is a **signaling cascade/network**, not a single molecule, so while it is commonly used as a therapeutic target in systems biology and oncology, it does not fit the strict definition of a molecular target (receptor, enzyme, etc.), and information may refer to multiple components (MEK1/2, ERK1/2, upstream, and downstream factors). - For structured data, information specific to MEK1/2 or ERK1/2 proteins may need to be separated appropriately. If you are seeking information on specific kinases (MEK1, MEK2, ERK1, ERK2), those can be separately detailed as molecular targets.

Other names

MAPK/ERK pathwayRas–Raf–MEK–ERK pathwayERK/MAPK pathway

MEK/ERK inhibitors block kinase activity to suppress pathway signaling, leading to reduced cell proliferation and increased apoptosis in tumor cells