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Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
08:45

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Published on: July 17, 2020

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Loss of Ptpn11 (Shp2) drives satellite cells into quiescence

Joscha Griger1, Robin Schneider1, Ines Lahmann1

  • 1Developmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, Germany.

Elife
|May 3, 2017
PubMed

Insights

The protein tyrosine phosphatase Ptpn11 (Shp2) is crucial for postnatal muscle stem cell activity. Loss of Shp2 halts proliferation, impairing muscle growth and repair in mice.

Area of Science:

  • Muscle biology
  • Cell signaling
  • Developmental biology

Background:

  • Skeletal muscle growth and repair depend on regulating myogenic progenitor and stem cells.
  • Non-receptor tyrosine phosphatase Ptpn11 (Shp2) transmits growth factor and cytokine signals.

Purpose of the Study:

  • Investigate the role of Ptpn11 in postnatal myogenesis.
  • Determine Ptpn11's function in muscle stem cell activity during growth and repair.

Main Methods:

  • Complex genetic analyses in mice
  • Biochemical studies
  • Pharmacological interference

Main Results:

  • Ptpn11 loss caused postnatal muscle stem cells to enter a resting state, halting proliferation.
  • This effect was specific to postnatal, not fetal, myogenic stem cells.
  • Ptpn11 ablation in stem cells severely impaired muscle repair due to reduced proliferation and survival.

Conclusions:

  • Ptpn11 signaling is essential for postnatal myogenesis and satellite cell activity.
  • Demonstrates a molecular difference in cell cycle control between fetal and postnatal myogenic stem cells.
  • Highlights Ptpn11's critical role in maintaining muscle stem cell function for growth and repair.
Keywords:
Ptpn11Shp2developmental biologymousequiescencesatellite cellsskeletal muscle growthskeletal muscle repairstem cells

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