Evidence map›Paper›PMID 27986865›Full record

ArticleBioscience reports2017

Cross-talks via mTORC2 can explain enhanced activation in response to insulin in diabetic patients.

Rasmus Magnusson, Mika Gustafsson, Gunnar Cedersund, Peter Strålfors, Elin Nyman

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    Review
  3. Article
  4. Finding new edges: systems approaches to MTOR signaling.Biochemical Society transactions · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. 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

5 authors at 1 institution in 1 country.

Rasmus MagnussonDepartment of Biomedical Engineering, Linköping University, Sweden.
Mika GustafssonDepartment of Physics, Chemistry and Biology, Linköping University, Sweden.
Gunnar CedersundDepartment of Biomedical Engineering, Linköping University, Sweden.
Peter StrålforsDepartment of Clinical and Experimental Medicine, Linköping University, Sweden.
Elin NymanDepartment of Biomedical Engineering, Linköping University, Sweden elin.nyman@liu.se.
Linköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular mechanisms of insulin resistance in Type 2 diabetes have been extensively studied in primary human adipocytes, and mathematical modelling has clarified the central role of attenuation of mammalian target of rapamycin (mTOR) complex 1 (mTORC1) activity in the diabetic state. Attenuation of mTORC1 in diabetes quells insulin-signalling network-wide, except for the mTOR in complex 2 (mTORC2)-catalysed phosphorylation of protein kinase B (PKB) at Ser

Indexed as

Signal Transduction3T3-L1 CellsAdaptor Proteins, Signal TransducingAdipocytesAnimalsDiabetes Mellitus, Type 2HumansInsulinInsulin ResistanceMechanistic Target of Rapamycin Complex 2MiceModels, BiologicalProto-Oncogene Proteins c-aktRibosomal Protein S6 KinasesAdaptor Proteins, Signal TransducingInsulinMAPKAP1 protein, humanMechanistic Target of Rapamycin Complex 2Proto-Oncogene Proteins c-aktRibosomal Protein S6 Kinasescomputational modelsmTORC1mTORC2protein kinase BSIN1Type 2 diabetes

Identifiers

PMID27986865
PMCPMC5271673
OpenAlexW2565099035

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.