ERK-Mediated Signal Transduction in Cell Migration

Extracellular signal-regulated kinase (ERK) occupies a central node in the mitogen-activated protein kinase (MAPK) cascade, translating a diverse array of extracellular cues into coordinated cytoskeletal and transcriptional responses that drive cell motility. Activation typically proceeds via growth factor engagement of receptor tyrosine kinases, recruitment of RAS and RAF kinases, and dual phosphorylation of ERK by MEK. Once activated, ERK translocates to multiple subcellular sites, phosphorylating effectors that regulate actin polymerisation, focal adhesion turnover and contractile machinery. Temporal and spatial dynamics of ERK activity—manifest as pulses, waves and sustained plateaus—enable cells to interpret complex guidance cues, integrate mechanical stresses and orchestrate both single-cell protrusion and collective migration. Mechanical inputs from substrate stiffness, cell–cell contacts and extracellular matrix tension modulate receptor clustering and feed into ERK activation, establishing bidirectional crosstalk between biochemical signalling and mechanotransduction. Through these interlinked processes, ERK governs embryonic development, tissue repair and pathological invasion, making its precise regulation a focal point for therapeutic intervention.

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ERK-Mediated Signal Transduction in Cell Migration publication trend

The graph below shows the total number of articles in erk-mediated signal transduction in cell migration across all publications each year (not limited to Nature Index journals).

Technical terms

ERK: A serine/threonine kinase in the MAPK cascade that phosphorylates substrates controlling cell movement and gene expression.

MAPK cascade: A hierarchical kinase module—comprising RAS, RAF, MEK and ERK—that relays extracellular signals to effector responses.

Mechanotransduction: The process by which cells convert mechanical stimuli (e.g. stretch or stiffness) into biochemical signals.

Lamellipodium: A flat, sheet-like protrusion enriched in branched actin that drives forward movement at a cell’s leading edge.

Focal adhesion: Multiprotein complexes that anchor the cytoskeleton to the extracellular matrix, transmitting traction forces during migration.

References

1. Emerging roles and mechanisms of ERK pathway mechanosensing. Cellular and Molecular Life Sciences (2023).
2. Stretching the limits of extracellular signal-related kinase (ERK) signaling — Cell mechanosensing to ERK activation. Current Opinion in Cell Biology (2023).
3. The MAPK/ERK channel capacity exceeds 6 bit/hour. PLOS Computational Biology (2023).
4. ERK signaling for cell migration and invasion. Frontiers in Molecular Biosciences (2022).
5. Substratum stiffness regulates Erk signaling dynamics through receptor-level control. Cell Reports (2021).
6. Redundant roles of EGFR ligands in the ERK activation waves during collective cell migration. Life Science Alliance (2021).