Evidence map›Paper›PMID 23839048›Full record

ArticleCell cycle (Georgetown, Tex.)2013

FKBPs and the Akt/mTOR pathway.

Felix Hausch, Christian Kozany, Marily Theodoropoulou, Anne-Katrin Fabian

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 77 citations in OpenAlex.

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  19. Rapamycin Promotes ROS-Mediated Cell DeathFrontiers in oncology · 2021
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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

4 authors at 1 institution in 1 country.

Felix HauschMax Planck Institute of Psychiatry; Munich, Germany.
Christian Kozany
Marily Theodoropoulou
Anne-Katrin Fabian
Max Planck Institute of Psychiatry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FK506-binding proteins (FKBP) belong to the immunophilin family and are best known for their ability to enable the immunosuppressive properties of FK506 and rapamycin. For rapamycin, this is achieved by inducing inhibitory ternary complexes with the kinase mTOR. The essential accessory protein for this gain-of-function was thought to be FKBP12. We recently showed that this view might be too restricted, since larger FK506-binding proteins can functionally substitute for FKBP12 in mammalian cells. Recent studies have also shown that FK506-binding proteins can modulate Akt-mTOR signaling in the absence of rapamycin. Here we discuss the role of FK506-binding proteins for the mechanism of rapamycin as well as their intrinsic actions on the Akt/mTOR pathway.

Indexed as

AnimalsHumansProto-Oncogene Proteins c-aktSignal TransductionSirolimusTacrolimus Binding ProteinsTOR Serine-Threonine KinasesProto-Oncogene Proteins c-aktSirolimusTacrolimus Binding ProteinsTOR Serine-Threonine KinasesAktFK506 binding proteinFKBPmTORPKBrapamycin

Identifiers

PMID23839048
PMCPMC3841315
OpenAlexW2003930211

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.