Evidence map›Paper›PMID 18957511›Full record

ArticleJournal of cell science2008

The role of Delta-like 1 shedding in muscle cell self-renewal and differentiation.

Danqiong Sun, Hui Li, Anna Zolkiewska

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  14. Regulation of DLK1 by the maternally expressed miR-379/miR-544 cluster may underlie callipyge polar overdominance inheritance.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
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  18. Numb-deficient satellite cells have regeneration and proliferation defects.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
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  20. Review
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

3 authors at 1 institution in 1 country.

Danqiong SunDepartment of Biochemistry, Kansas State University, Manhattan, KS 66506, USA.
Hui Li
Anna Zolkiewska
Kansas State University · US

Funding

Molecular Analysis of Metalloprotease Disintegrin ADAM12R01GM065528 · NIGMS · KANSAS STATE UNIVERSITY · PI ZOLKIEWSKA, ANNA · 2004 to 2007
$860k
NIGMS NIH HHS GM065528NIGMS NIH HHS R01 GM065528
6 · The paper itself

Abstract

Myogenic cells have the ability to adopt two divergent fates upon exit from the cell cycle: differentiation or self-renewal. The Notch signaling pathway is a well-known negative regulator of myogenic differentiation. Using mouse primary myoblasts cultured in vitro or C2C12 myogenic cells, we found that Notch activity is essential for maintaining the expression of Pax7, a transcription factor associated with the self-renewal lineage, in quiescent undifferentiated myoblasts after they exit the cell cycle. Stimulation of the Notch pathway by expression of a constitutively active Notch-1, or co-culture of myogenic cells with CHO cells transfected with Delta like-1 (DLL1), increases the level of Pax7. DLL1, a ligand for Notch receptor, is shed by ADAM metalloproteases in a pool of Pax7+ C2C12 reserve cells, but it remains intact in differentiated myotubes. DLL1 shedding changes the receptor/ligand ratio and modulates the level of Notch signaling. Inhibition of DLL1 cleavage by a soluble, dominant-negative mutant form of ADAM12 leads to elevation of Notch signaling, inhibition of differentiation, and expansion of the pool of self-renewing Pax7+/MyoD- cells. These results suggest that ADAM-mediated shedding of DLL1 in a subset of cells during myogenic differentiation in vitro contributes to downregulation of Notch signaling in neighboring cells and facilitates their progression into differentiation. We propose that the proteolytic processing of DLL1 helps achieve an asymmetry in Notch signaling in initially equivalent myogenic cells and helps sustain the balance between differentiation and self-renewal.

Indexed as

Cell DifferentiationAnimalsCalcium-Binding ProteinsCell LineCells, CulturedIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMyoblastsMyocytes, Smooth MusclePAX7 Transcription FactorSignal TransductionCalcium-Binding ProteinsDlk1 protein, mouseIntercellular Signaling Peptides and ProteinsPax7 protein, mousePAX7 Transcription Factor

Identifiers

PMID18957511
PMCPMC2636845
OpenAlexW2138471981

What OpenQuestion holds

Textmetadata
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.