Evidence map›Paper›PMID 24047696›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Cellular senescence or EGFR signaling induces Interleukin 6 (IL-6) receptor expression controlled by mammalian target of rapamycin (mTOR).

Christoph Garbers, Fabian Kuck, Samadhi Aparicio-Siegmund, Kirstin Konzak, Mareike Kessenbrock, Annika Sommerfeld, Dieter Häussinger, Philipp A Lang, Dirk Brenner, Tak W Mak and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-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

40 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Cellular Senescence, Inflammation, and Cancer in the Gastrointestinal Tract.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Phosphate and Cellular Senescence.Advances in experimental medicine and biology · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Protective effects ofInternational journal of molecular medicine · 2021
    Article
  17. Article
  18. Article
  19. Review
  20. CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
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

15 authors at 6 institutions in 5 countries.

Christoph GarbersInstitute of Biochemistry and Molecular Biology II; Medical Faculty; Heinrich-Heine-University; Düsseldorf, Germany.
Fabian Kuck
Samadhi Aparicio-Siegmund
Kirstin Konzak
Mareike Kessenbrock
Annika Sommerfeld
Dieter Häussinger
Philipp A Lang
Dirk Brenner
Tak W Mak
Stefan Rose-John
Frank Essmann
Klaus Schulze-Osthoff
Roland P Piekorz
Jürgen Scheller
Heinrich Heine University Düsseldorf · DEFaculty (United Kingdom) · GBUniversity of Tübingen · DEHealth Net · USKiel University · DEOntario Institute for Cancer Research · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 6 (IL-6) signaling plays a role in inflammation, cancer, and senescence. Here, we identified soluble IL-6 receptor (sIL-6R) as a member of the senescence-associated secretory phenotype (SASP). Senescence-associated sIL-6R upregulation was mediated by mammalian target of rapamycin (mTOR). sIL-6R was mainly generated by a disintegrin and metalloprotease 10 (ADAM10)-dependent ectodomain shedding to enable IL-6 trans-signaling. In vivo, heterozygous PTEN-knockout mice exhibited higher mTOR activity and increased sIL-6R levels. Moreover, aberrant EGF receptor (EGFR) activation triggered IL-6 synthesis. In analogy to senescence, EGFR-induced activation of mTOR also induced IL-6R expression and sIL-6R generation. Hence, mTOR activation reprograms IL-6 non-responder cells into IL-6 responder cells. Our data suggest that mTOR serves as a central molecular switch to facilitate cellular IL-6 classic and trans-signaling via IL-6R upregulation with direct implications for cellular senescence and tumor development.

Indexed as

Gene Expression Regulation, NeoplasticADAM10 ProteinADAM ProteinsAmyloid Precursor Protein SecretasesAnimalsCarrier ProteinsCell LineCell Transformation, NeoplasticCellular SenescenceErbB ReceptorsFetal ProteinsHumansInterleukin-6Membrane ProteinsMiceMice, KnockoutADAM10 ProteinAdam10 protein, mouseADAM ProteinsAmyloid Precursor Protein SecretasesCarrier ProteinsEGFR protein, mouseErbB ReceptorsFetal ProteinsInterleukin-6Membrane ProteinsMicrotubule-Associated ProteinsmTOR protein, mousePTEN PhosphohydrolasePTEN protein, humanReceptors, Interleukin-6RNA, Small InterferingTACC3 protein, mouseTOR Serine-Threonine KinasesEGFRInterleukin 6Interleukin 6-ReceptormTORSASPsenescence

Identifiers

PMID24047696
PMCPMC3895430
OpenAlexW2074934443

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.