Evidence map›Paper›PMID 22045613›Full record

ArticleStem cells (Dayton, Ohio)2012

Notch signaling is necessary to maintain quiescence in adult muscle stem cells.

Christopher R R Bjornson, Tom H Cheung, Ling Liu, Pinky V Tripathi, Katherine M Steeper, Thomas A Rando

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 342 papers.

0numbers the graph read from it
0cells of the map it votes in
342citing papers in PubMed
11.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

342 citing papers in PubMed, 549 citations in OpenAlex.

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  7. A Myocyte-Enriched Long Non-Coding RNA NRMLncR Enhances Myogenesis in Mouse.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  20. bioRxiv : the preprint server for biology · 2026
    Article

282 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Christopher R R BjornsonDepartment of Neurology and Neurological Sciences, Stanford University, Stanford, California, USA.
Tom H Cheung
Ling Liu
Pinky V Tripathi
Katherine M Steeper
Thomas A Rando
Stanford University · USVA Palo Alto Health Care System · US

Funding

Wnt signaling in muscle stem cell agingP01AG036695 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARGARET A. GOODELL · 2011 to 2026
$29.3M
NIH Director's Pioneer Award (RMI)DP1OD000392 · OD · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2005 to 2009
$3.3M
Notch Signaling and Satellite Cell ActivationR37AG023806 · NIA · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2010 to 2019
$2.9M
Molecular Regulation of Myogenic DifferentiationR01AR056849 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI RANDO, THOMAS A. · 2009 to 2013
$1.5M
Notch Signaling and Satellite Cell ActivationR01AG023806 · NIA · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2005 to 2009
$1.2M
NIAMS NIH HHS R01 AR056849NIA NIH HHS P01 AG036695NIA NIH HHS R01 AG023806NIA NIH HHS R37 AG023806NIA NIH HHS R37 AG23806NIH HHS DP1 OD000392
6 · The paper itself

Abstract

Satellite cells (SCs) are myogenic stem cells found in skeletal muscle that function to repair tissue damaged by injury or disease. SCs are quiescent at rest, although the signaling pathways required to maintain quiescence are unknown. Using a transgenic Notch reporter mouse and quantitative reverse-transcription polymerase chain reaction analysis of Notch target genes, we determined that Notch signaling is active in quiescent SCs. SC-specific deletion of recombining binding protein-Jκ (RBP-Jκ), a nuclear factor required for Notch signaling, resulted in the depletion of the SC pool and muscles that lacked any ability to regenerate in response to injury. SC depletion was not due to apoptosis. Rather, RBP-Jκ-deficient SCs spontaneously activate, fail to self-renew, and undergo terminal differentiation. Intriguingly, most of the cells differentiate without first dividing. They then fuse with adjacent myofibers, leading to the gradual disappearance of SCs from the muscle. These results demonstrate the requirement of Notch signaling for the maintenance of the quiescent state and for muscle stem cell homeostasis by the regulation of self-renewal and differentiation, processes that are all critical for normal postnatal myogenesis.

Indexed as

Cell Cycle CheckpointsSignal TransductionAdult Stem CellsAnimalsApoptosisCell LineageCell ProliferationCells, CulturedImmunoglobulin J Recombination Signal Sequence-Binding ProteinMiceMice, TransgenicMuscle DevelopmentMuscle, SkeletalPAX7 Transcription FactorReceptors, NotchImmunoglobulin J Recombination Signal Sequence-Binding ProteinPax7 protein, mousePAX7 Transcription FactorRbpj protein, mouseReceptors, Notch

Identifiers

PMID22045613
PMCPMC3384696
OpenAlexW2015185372

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

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.