ArticleeLife2017
Loss of Ptpn11 (Shp2) drives satellite cells into quiescence.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Renalase knockdown inhibits proliferation of mouse satellite cells.Molecular biology reports · 2026Article
- Article
- Neurofibromin 1 controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors.Nature communications · 2024Article
- Insm1 regulates mTEC development and immune tolerance.Cellular & molecular immunology · 2023Article
- From Stem to Sternum: The Role of Shp2 in the Skeleton.Calcified tissue international · 2023Review
- Exploring the cause of the dual allosteric targeted inhibition attaching to allosteric sites enhancing SHP2 inhibition.Molecular diversity · 2022Article
- Injury-induced Erk1/2 signaling tissue-specifically interacts with CaCell calcium · 2022Article
- Actions and interactions of IGF-I and MMPs during muscle regeneration.Seminars in cell & developmental biology · 2021Review
- SHP2 inhibition enhances the anticancer effect of Osimertinib in EGFR T790M mutant lung adenocarcinoma by blocking CXCL8 loop mediated stemness.Cancer cell international · 2021Article
- Article
- Hepatocyte growth factor acts as a mitogen for equine satellite cells via protein kinase C δ-directed signaling.Journal of animal science · 2018Article
- Shp2-Mitogen-Activated Protein Kinase Signaling Drives Proliferation during Zebrafish Embryo Caudal Fin Fold Regeneration.Molecular and cellular biology · 2018Article
- SHP2-Mediated Signal Networks in Stem Cell Homeostasis and Dysfunction.Stem cells international · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The equilibrium between proliferation and quiescence of myogenic progenitor and stem cells is tightly regulated to ensure appropriate skeletal muscle growth and repair. The non-receptor tyrosine phosphatase Ptpn11 (Shp2) is an important transducer of growth factor and cytokine signals. Here we combined complex genetic analyses, biochemical studies and pharmacological interference to demonstrate a central role of Ptpn11 in postnatal myogenesis of mice. Loss of Ptpn11 drove muscle stem cells out of the proliferative and into a resting state during muscle growth. This Ptpn11 function was observed in postnatal but not fetal myogenic stem cells. Furthermore, muscle repair was severely perturbed when Ptpn11 was ablated in stem cells due to a deficit in stem cell proliferation and survival. Our data demonstrate a molecular difference in the control of cell cycle withdrawal in fetal and postnatal myogenic stem cells, and assign to Ptpn11 signaling a key function in satellite cell activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.