Evidence map›Paper›PMID 20682446›Full record

ArticleCell stem cell2010

Transient inactivation of Rb and ARF yields regenerative cells from postmitotic mammalian muscle.

Kostandin V Pajcini, Stephane Y Corbel, Julien Sage, Jason H Pomerantz, Helen M Blau

Abstract read
In one paragraph

Article in Cell stem cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
18.1field-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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Specific cell states underlie complex tissue regeneration in spiny mice.bioRxiv : the preprint server for biology · 2025
    Article
  7. Hallmarks of regeneration.Cell stem cell · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Transit Amplifying Cells (TACs): a still not fully understood cell population.Frontiers in bioengineering and biotechnology · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Role ofBiomolecules · 2021
    Article
  20. Review

49 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

5 authors at 3 institutions in 1 country.

Kostandin V PajciniBaxter Laboratory for Stem Cell Biology, Department of Microbiology & Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Stephane Y Corbel
Julien Sage
Jason H Pomerantz
Helen M Blau
Stanford University · USBaxter (United States) · USPediatrics and Genetics · US

Funding

MOLECULAR BASIS OF HOST-PARASITE INTERACTIONT32AI007328 · NIAID · STANFORD UNIVERSITY · PI JUSTIN L SONNENBURG · 1987 to 2026
$11.9M
Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
Stem Cells for Brain and BrawnR01AG020961 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2002 to 2019
$5.0M
ACTIVATORS OF MUSCLE GENESR01AG009521 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 1990 to 2014
$4.7M
TRAINING IN NEONATAL BIOLOGYT32HD007249 · NICHD · STANFORD UNIVERSITY · PI STEVENSON, DAVID K · 1985 to 2013
$4.4M
Regulation of Hematopoietic Stem Cell Fate in Bioengineered NichesR01HL096113 · NHLBI · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2009 to 2013
$2.7M
ACTIVATORS OF HUMAN MUSCLE GENESR37AG009521 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 1995 to 2004
$2.3M
Mechanisms Underlying Plasticity of Gene ExpressionF32AR051678 · NIAMS · STANFORD UNIVERSITY · PI POMERANTZ, JASON H · 2004 to 2005
$104k
NHLBI NIH HHS HL096113NHLBI NIH HHS R01 HL096113NHLBI NIH HHS U01 HL100397NIAID NIH HHS 5T32 AI07328NIAID NIH HHS T32 AI007328NIAMS NIH HHS F32 AR051678NIAMS NIH HHS F32 AR051678-01NIA NIH HHS AG009521NIA NIH HHS AG020961NIA NIH HHS R01 AG009521NIA NIH HHS R01 AG020961NIA NIH HHS R37 AG009521NICHD NIH HHS 2T32 HD007249NICHD NIH HHS 5T32 HD007249NICHD NIH HHS T32 HD007249
6 · The paper itself

Abstract

An outstanding biological question is why tissue regeneration in mammals is limited, whereas urodele amphibians and teleost fish regenerate major structures, largely by cell cycle reentry. Upon inactivation of Rb, proliferation of postmitotic urodele skeletal muscle is induced, whereas in mammalian muscle this mechanism does not exist. We postulated that a tumor suppressor present in mammals but absent in regenerative vertebrates, the Ink4a product ARF (alternative reading frame), is a regeneration suppressor. Concomitant inactivation of Arf and Rb led to mammalian muscle cell cycle reentry, loss of differentiation properties, and upregulation of cytokinetic machinery. Single postmitotic myocytes were isolated by laser micro-dissection-catapulting, and transient suppression of Arf and Rb yielded myoblast colonies that retained the ability to differentiate and fuse into myofibers upon transplantation in vivo. These results show that differentiation of mammalian cells is reversed by inactivation of Arf and Rb and support the hypothesis that Arf evolved at the expense of regeneration.

Indexed as

MitosisAnimalsCell DedifferentiationCell NucleusCell ProliferationCells, CulturedClone CellsCyclin-Dependent Kinase Inhibitor p16CytokinesisLasersMammalsMiceMicrodissectionMuscle CellsMuscle Fibers, SkeletalMusclesCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16Retinoblastoma ProteinRNA, Small Interfering

Identifiers

PMID20682446
PMCPMC2919350
OpenAlexW2151037856

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.