Evidence map›Paper›PMID 29641997›Full record

ArticleCell reports2018

MYC Releases Early Reprogrammed Human Cells from Proliferation Pause via Retinoblastoma Protein Inhibition.

Tim A Rand, Kenta Sutou, Koji Tanabe, Daeun Jeong, Masaki Nomura, Fumiyo Kitaoka, Emi Tomoda, Megumi Narita, Michiko Nakamura, Masahiro Nakamura and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  9. A neural stem cell paradigm of pediatric hydrocephalus.Cerebral cortex (New York, N.Y. : 1991) · 2023
    Article
  10. International journal of biological sciences · 2023
    Article
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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

14 authors at 3 institutions in 2 countries.

Tim A RandGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
Kenta SutouDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Koji TanabeInstitute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Daeun JeongGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
Masaki NomuraDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Fumiyo KitaokaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Emi TomodaGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
Megumi NaritaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Michiko NakamuraDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Masahiro NakamuraDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Akira WatanabeDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Eric RulifsonDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Shinya YamanakaGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA; Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan; Department of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: syamanaka@gladstone.ucsf.edu.
Kazutoshi TakahashiGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA; Department of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan. Electronic address: kazutoshi.takahashi@gladstone.ucsf.edu.
Kyoto University · JPGladstone Institutes · USStanford University · US

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Monica Gandhi · 1988 to 2026
$93.6M
The Epigenetic Landscape of Heart DevelopmentU01HL098179 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI BOYER, LAURIE A, BRUNEAU, BENOIT GAETAN · 2009 to 2014
$10.0M
Induced Pluripotent Stem Cells in the Understanding and Treatment of Heart DiseasU01HL100406 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI BRUNEAU, BENOIT GAETAN, CONKLIN, BRUCE R · 2009 to 2015
$9.4M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
NCRR NIH HHS C06 RR018928NHLBI NIH HHS U01 HL098179NHLBI NIH HHS U01 HL100406NIAID NIH HHS P30 AI027763
6 · The paper itself

Abstract

Here, we report that MYC rescues early human cells undergoing reprogramming from a proliferation pause induced by OCT3/4, SOX2, and KLF4 (OSK). We identified ESRG as a marker of early reprogramming cells that is expressed as early as day 3 after OSK induction. On day 4, ESRG positive (+) cells converted to a TRA-1-60 (+) intermediate state. These early ESRG (+) or TRA-1-60 (+) cells showed a proliferation pause due to increased p16INK4A and p21 and decreased endogenous MYC caused by OSK. Exogenous MYC did not enhance the appearance of initial reprogramming cells but instead reactivated their proliferation and improved reprogramming efficiency. MYC increased expression of LIN41, which potently suppressed p21 post-transcriptionally. MYC suppressed p16 INK4A. These changes inactivated retinoblastoma protein (RB) and reactivated proliferation. The RB-regulated proliferation pause does not occur in immortalized fibroblasts, leading to high reprogramming efficiency even without exogenous MYC.

Indexed as

Cellular ReprogrammingAntigens, SurfaceCell LineCell ProliferationCyclin-Dependent Kinase Inhibitor p16HumansInduced Pluripotent Stem CellsKruppel-Like Factor 4PhosphorylationProteoglycansProto-Oncogene Proteins c-mycRetinoblastoma ProteinRNA InterferenceRNA, Small InterferingTranscription FactorsTripartite Motif ProteinsAntigens, SurfaceCyclin-Dependent Kinase Inhibitor p16KLF4 protein, humanKruppel-Like Factor 4ProteoglycansProto-Oncogene Proteins c-mycRetinoblastoma ProteinRNA, Small InterferingTRA-1-60 antigen, humanTranscription FactorsTRIM71 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligasesimmortalizationinduced pluripotent stem cellLIN41MYCpluripotencypost-transcriptional regulationproliferationreprogrammingsenescence

Identifiers

PMID29641997
PMCPMC8241223
OpenAlexW2797306832

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.