Evidence map›Paper›PMID 21633171›Full record

ArticleThe Journal of clinical investigation2011

S6 kinase 1 is required for rapamycin-sensitive liver proliferation after mouse hepatectomy.

Catherine Espeillac, Claudia Mitchell, Séverine Celton-Morizur, Céline Chauvin, Vonda Koka, Cynthia Gillet, Jeffrey H Albrecht, Chantal Desdouets, Mario Pende

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Review
  3. mRNA translational control of regeneration.Current opinion in genetics & development · 2025
    Review
  4. Review
  5. Review
  6. Using different zebrafish models to explore liver regeneration.Frontiers in cell and developmental biology · 2024
    Review
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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

9 authors at 4 institutions in 2 countries.

Catherine EspeillacInserm, U845, Paris, France.
Claudia Mitchell
Séverine Celton-Morizur
Céline Chauvin
Vonda Koka
Cynthia Gillet
Jeffrey H Albrecht
Chantal Desdouets
Mario Pende
Université Paris Cité · FRInserm · FRCentre National de la Recherche Scientifique · FRHennepin County Medical Center · US

Funding

The Cyclin D1/CDK4 Complex in Hepatocyte ProliferationR01DK054921 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALBRECHT, JEFFREY H · 1998 to 2017
$4.5M
NIDDK NIH HHS DK54921NIDDK NIH HHS R01 DK054921
6 · The paper itself

Abstract

Rapamycin is an antibiotic inhibiting eukaryotic cell growth and proliferation by acting on target of rapamycin (TOR) kinase. Mammalian TOR (mTOR) is thought to work through 2 independent complexes to regulate cell size and cell replication, and these 2 complexes show differential sensitivity to rapamycin. Here we combine functional genetics and pharmacological treatments to analyze rapamycin-sensitive mTOR substrates that are involved in cell proliferation and tissue regeneration after partial hepatectomy in mice. After hepatectomy, hepatocytes proliferated rapidly, correlating with increased S6 kinase phosphorylation, while treatment with rapamycin derivatives impaired regeneration and blocked S6 kinase activation. In addition, genetic deletion of S6 kinase 1 (S6K1) caused a delay in S phase entry in hepatocytes after hepatectomy. The proliferative defect of S6K1-deficient hepatocytes was cell autonomous, as it was also observed in primary cultures and hepatic overexpression of S6K1-rescued proliferation. We found that S6K1 controlled steady-state levels of cyclin D1 (Ccnd1) mRNA in liver, and cyclin D1 expression was required to promote hepatocyte cell cycle. Notably, in vivo overexpression of cyclin D1 was sufficient to restore the proliferative capacity of S6K-null livers. The identification of an S6K1-dependent mechanism participating in cell proliferation in vivo may be relevant for cancer cells displaying high mTOR complex 1 activity and cyclin D1 accumulation.

Indexed as

AnimalsAntibiotics, AntineoplasticCell CycleCell ProliferationCells, CulturedCyclin D1GenotypeHepatectomyHepatocytesIsoenzymesLiverLiver RegenerationMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutAntibiotics, AntineoplasticCyclin D1IsoenzymesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProteinsRibosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouseSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID21633171
PMCPMC3223822
OpenAlexW2044138231

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.