ERK and cell death: ERK1/2 in neuronal death

Related Experiment Video

Updated: Jun 19, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Srinivasa Subramaniam1, Klaus Unsicker

  • 1Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ssubram9@jhmi.edu

The FEBS Journal
|October 22, 2009
PubMed

Insights

Extracellular signal-regulated kinase (ERK) signaling influences neuronal death, particularly in neurodegenerative diseases. The activity level and duration of ERK1/2 determine its role in cell fate.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Neuroscience

Background:

  • Extracellular signal-regulated kinase (ERK) is a key regulator of cellular processes.
  • ERK1/2 activation is implicated in neuronal function and dysfunction.
  • Dysregulation of ERK signaling is observed in various neurodegenerative conditions.

Purpose of the Study:

  • To review the role of ERK1/2 in neuronal death.
  • To elucidate the mechanisms by which ERK1/2 mediates neuronal death.
  • To highlight the significance of ERK1/2 activity in neurodegeneration.

Main Methods:

  • Literature review of recent studies on ERK1/2 and neuronal death.
  • Analysis of experimental evidence linking ERK1/2 activity to cell death pathways.
  • Synthesis of mechanistic insights into ERK1/2-mediated neuronal apoptosis.

Main Results:

  • ERK1/2 plays a critical role in promoting neuronal death across different neuronal systems.
  • The magnitude and duration of ERK1/2 activity are crucial determinants of its cellular outcome.
  • Specific signaling pathways activated by ERK1/2 contribute to neuronal demise.

Conclusions:

  • ERK1/2 is a significant mediator of neuronal death, especially relevant in neurodegenerative diseases.
  • Understanding ERK1/2 mechanisms offers potential therapeutic targets for neuroprotection.
  • Modulating ERK1/2 activity may represent a strategy to combat neuronal loss.

More Related Videos

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...