Evidence map›Paper›PMID 28007786›Full record

ArticleGenes & development2016

Myc/Mycn-mediated glycolysis enhances mouse spermatogonial stem cell self-renewal.

Mito Kanatsu-Shinohara, Takashi Tanaka, Narumi Ogonuki, Atsuo Ogura, Hiroko Morimoto, Pei Feng Cheng, Robert N Eisenman, Andreas Trumpp, Takashi Shinohara

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Metabolic transitions define spermatogonial stem cell maturation.Human reproduction (Oxford, England) · 2022
    Pooled it
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  9. The ChickenGenes · 2024
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3 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

9 authors at 5 institutions in 3 countries.

Mito Kanatsu-ShinoharaDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Takashi TanakaDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Narumi OgonukiBioresource Center, RIKEN, Tsukuba 305-0074, Japan.
Atsuo OguraBioresource Center, RIKEN, Tsukuba 305-0074, Japan.
Hiroko MorimotoDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Pei Feng ChengDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Robert N EisenmanDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Andreas TrumppDivision of Stem Cells and Cancer, Deutsches Krebsforshungszentrum (DKFZ), 69120 Heidelberg, Germany.
Takashi ShinoharaDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Kyoto University · JPFred Hutch Cancer Center · USRIKEN BioResource Research Center · JPDKFZ-ZMBH Alliance · DEJapan Science and Technology Agency · JP

Funding

MYC ONCOPROTEIN FUNCTIONR01CA057138 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1991 to 2018
$4.9M
NCI NIH HHS R01 CA057138
6 · The paper itself

Abstract

Myc plays critical roles in the self-renewal division of various stem cell types. In spermatogonial stem cells (SSCs), Myc controls SSC fate decisions because Myc overexpression induces enhanced self-renewal division, while depletion of Max, a Myc-binding partner, leads to meiotic induction. However, the mechanism by which Myc acts on SSC fate is unclear. Here we demonstrate a critical link between Myc/Mycn gene activity and glycolysis in SSC self-renewal. In SSCs, Myc/Mycn are regulated by Foxo1, whose deficiency impairs SSC self-renewal. Myc/Mycn-deficient SSCs not only undergo limited self-renewal division but also display diminished glycolytic activity. While inhibition of glycolysis decreased SSC activity, chemical stimulation of glycolysis or transfection of active Akt1 or Pdpk1 (phosphoinositide-dependent protein kinase 1 ) augmented self-renewal division, and long-term SSC cultures were derived from a nonpermissive strain that showed limited self-renewal division. These results suggested that Myc-mediated glycolysis is an important factor that increases the frequency of SSC self-renewal division.

Indexed as

3-Phosphoinositide-Dependent Protein KinasesAnimalsCell DivisionCell ProliferationCell Self RenewalGene Expression Regulation, DevelopmentalGene Knockout TechniquesGlycolysisMaleMiceMice, Inbred C57BLN-Myc Proto-Oncogene ProteinProto-Oncogene Proteins c-mycRNA Splicing FactorsSpermatogoniaStem Cells3-Phosphoinositide-Dependent Protein KinasesMYCN protein, mouseN-Myc Proto-Oncogene ProteinPdpk1 protein, mouseProto-Oncogene Proteins c-mycRbfox1 protein, mouseRNA Splicing FactorsglycolysisMycself-renewalspermatogenesisspermatogonial stem cells

Identifiers

PMID28007786
PMCPMC5204355
OpenAlexW2566311548

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.