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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Related Experiment Video

Updated: Dec 25, 2025

Cell Sorting of Neural Stem and Progenitor Cells from the Adult Mouse Subventricular Zone and Live-imaging of their Cell Cycle Dynamics
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Elevated p38MAPK activity promotes neural stem cell aging.

Leire Moreno-Cugnon1, Olatz Arrizabalaga1, Irantzu Llarena2

  • 1Biodonostia Health Research Institute, Group of Cellular Oncology, San Sebastian, Spain.

Aging
|April 4, 2020
PubMed
Summary

Increased p38MAPK activity impairs neural stem cell (NSC) function during aging. Inhibiting this pathway rejuvenates NSC activity, revealing a key factor in brain aging and neurogenesis decline.

Keywords:
agingneural stem cellp38MAPKpharmacological inhibition

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Area of Science:

  • Neuroscience
  • Stem Cell Biology
  • Aging Research

Background:

  • Neural stem cell (NSC) dysfunction contributes to cognitive decline and neurodegenerative diseases with age.
  • The p38MAPK signaling pathway's role in aging neural stem cells is not well understood.

Purpose of the Study:

  • To investigate the role of p38MAPK activity in age-related neural stem cell dysfunction.
  • To determine if inhibiting p38MAPK can restore neural stem cell function in aging.

Main Methods:

  • Assessed p38MAPK activity in neural stem cells from aged and young mice.
  • Utilized pharmacological inhibition of p38MAPK in vitro.
  • Evaluated neural stem cell activity and homeostasis.

Main Results:

  • p38MAPK activity was found to increase in neural stem cells with age in the subventricular zone (SVZ).
  • Pharmacological inhibition of p38MAPK successfully rejuvenated neural stem cell activity in vitro.
  • The study identified a cell-autonomous role for elevated p38MAPK in diminishing NSC homeostasis during aging.

Conclusions:

  • Increased p38MAPK activity is a key driver of neural stem cell aging.
  • Targeting p38MAPK offers a potential therapeutic strategy for age-related cognitive decline and neurodegeneration.