Evidence map›Paper›PMID 10373556›Full record

ArticleMolecular and cellular biology1999

Cell cycle withdrawal promotes myogenic induction of Akt, a positive modulator of myocyte survival.

Y Fujio, K Guo, T Mano, Y Mitsuuchi, J R Testa, K Walsh

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 217 citations in OpenAlex.

  1. Article
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  6. Thioredoxin mitigates HFEBS open bio · 2020
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  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. miR-340 Inhibits Proliferation and Induces Apoptosis in Gastric Cancer Cell Line SGC-7901, Possibly via the AKT Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  17. Article
  18. Article
  19. Stem cell death and survival in heart regeneration and repair.Apoptosis : an international journal on programmed cell death · 2016
    Review
  20. Article

15 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.

Y FujioDivision of Cardiovascular Research, St. Elizabeth's Medical Center of Boston, Tufts University School of Medicine, Boston, Massachusetts 02135, USA.
K Guo
T Mano
Y Mitsuuchi
J R Testa
K Walsh
Tufts University · USFox Chase Cancer Center · US

Funding

REGULATION OF VESSEL WALL APOPTOSISR37AG015052 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2003 to 2012
$4.0M
TRANSLATION INHIBITORY RNA SPECIESP01HD023681 · NICHD · TUFTS UNIVERSITY BOSTON · PI LINSENMAYER, THOMAS FRANK · 1988 to 2003
$3.5M
REGULATION OF VESSEL WALL APOPTOSISR01AG015052 · NIA · CARITAS ST. ELIZABETH'S MEDICAL CENTER · PI WALSH, KENNETH · 1998 to 2002
$1.0M
TRANSCRIPTIONAL CONTROL OF CARDIOVASCULAR PATHOLOGYR01HL050692 · NHLBI · CARITAS ST. ELIZABETH'S MEDICAL CENTER · PI WALSH, KENNETH · 1993 to 2001
$660k
NHLBI NIH HHS HL50692NIA NIH HHS AG15052NIA NIH HHS R01 AG015052NIA NIH HHS R37 AG015052NICHD NIH HHS HD23681NICHD NIH HHS P01 HD023681
6 · The paper itself

Abstract

During myogenesis, proliferating myoblasts withdraw from the cell cycle, acquire an apoptosis-resistant phenotype, and differentiate into myotubes. Previous studies indicate that myogenic induction of the cyclin-dependent kinase inhibitor p21 results in an inhibition of apoptotic cell death in addition to its role as a negative cell cycle regulator. Here we demonstrate that the protein encoded by the Akt proto-oncogene is induced in C2C12 cells during myogenic differentiation with a corresponding increase in kinase activity. In differentiating cultures, expression of dominant-negative forms of Akt increase the frequency of cell death whereas expression of wild-type Akt protects against death, indicating that Akt is a positive modulator of myocyte survival. Antisense oligonucleotides against p21 block cell cycle withdrawal, inhibit Akt induction, and enhance cell death in differentiating myocyte cultures. Adenovirus-mediated transfer of wild-type or constitutively active Akt constructs confer partial resistance to cell death under conditions where cell cycle exit is blocked by the antisense oligonucleotides. Collectively, these data indicate that cell cycle withdrawal facilitates the induction of Akt during myogenesis, promoting myocyte survival.

Indexed as

Cell CycleProtein Serine-Threonine KinasesAdenoviruses, HumanAnimalsCell DifferentiationCell LineCell SurvivalCyclin-Dependent Kinase Inhibitor p21CyclinsGenetic VectorsGene Transfer TechniquesMiceMitosisMusclesProtein-Tyrosine KinasesProto-Oncogene MasCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21CyclinsMAS1 protein, humanProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID10373556
PMCPMC84350
OpenAlexW2150684620

What OpenQuestion holds

Textmetadata
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.