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ERK1/2 in immune signalling.

Richard M Lucas1, Lin Luo1, Jennifer L Stow1

  • 1Institute for Molecular Bioscience (IMB) and Centre for Inflammation and Disease Research, The University of Queensland, St Lucia, QLD 4072, Australia.

Biochemical Society Transactions
|October 25, 2022
PubMed
Summary
This summary is machine-generated.

Extracellular signal-related kinases 1 and 2 (ERK1/2) are key in cell signaling and inflammation. Dysfunctional ERK1/2 pathways are linked to inflammatory diseases, suggesting therapeutic potential.

Keywords:
Toll-like receptorscytokinesextracellular signal-regulated kinasesinflammationinnate immunityreceptor signalling

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Area of Science:

  • Cellular Biology
  • Immunology
  • Molecular Biology

Background:

  • Extracellular signal-related kinases 1 and 2 (ERK1/2) are terminal components of the mitogen-activated protein kinase (MAPK) cascade, regulating cell behavior and fate.
  • ERK1/2 activation is crucial downstream of immune receptors, driving inflammatory gene expression in response to infection and tissue damage.
  • Toll-like receptor (TLR) pathways extensively studied ERK1/2 activation in innate immune cells.

Approach:

  • This review summarizes ERK1/2 activation in growth factor receptor pathways.
  • It discusses ERK1/2 roles in immune cell signaling, focusing on downstream effects of TLRs.
  • Emerging research on dysfunctional ERK1/2 signaling in inflammatory diseases is examined.

Key Points:

  • ERK1/2 pathways are integral to diverse signaling cascades influencing cell behavior.
  • ERK1/2 plays a critical role in innate immunity, mediating inflammatory gene expression via TLRs.
  • Evidence suggests ERK1/2 pathway dysfunction contributes to inflammatory diseases.

Conclusions:

  • Understanding ERK1/2 activation in both growth factor and immune signaling is essential.
  • Targeting ERK1/2 pathways presents a potential therapeutic strategy for managing inflammatory conditions.