Evidence map›Paper›PMID 23787999›Full record

ArticleCell death and differentiation2013

Akt1 is the principal Akt isoform regulating apoptosis in limiting cytokine concentrations.

B D Green, A M Jabbour, J J Sandow, C D Riffkin, D Masouras, C P Daunt, M Salmanidis, G Brumatti, B A Hemmings, M A Guthridge and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Akt isoform specificity drives intrinsic immune regulation during HSV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. AKT Isoforms in Macrophage Activation, Polarization, and Survival.Current topics in microbiology and immunology · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 2 countries.

B D GreenCell Signalling and Cell Death Division, Walter and Eliza Hall Institute of Medical Research, Royal Parade, Parkville, Victoria 3052, Australia.
A M Jabbour
J J Sandow
C D Riffkin
D Masouras
C P Daunt
M Salmanidis
G Brumatti
B A Hemmings
M A Guthridge
R B Pearson
P G Ekert
Walter and Eliza Hall Institute of Medical Research · AUUniversity of Melbourne · AUFriedrich Miescher Institute · CHMonash University · AUMurdoch Children's Research Institute · AURoyal Children's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation of the Akt signalling in response to cytokine receptor signalling promotes protein synthesis, cellular growth and proliferation. To determine the role of Akt in interleukin-3 (IL-3) signalling, we generated IL-3-dependent myeloid cell lines from mice lacking Akt1, Akt2 or Akt3. Akt1 deletion resulted in accelerated apoptosis at low concentrations of IL-3. Expression of constitutively active Akt1 was sufficient to delay apoptosis in response to IL-3 withdrawal, but not sufficient to induce proliferation in the absence of IL-3. Akt1 prolonged survival of Bim- or Bad-deficient cells, but not cells lacking Puma, indicating that Akt1-dependent repression of apoptosis was in part dependent on Puma and independent of Bim or Bad. Our data show that a key role of Akt1 during IL-3 signalling is to repress p53-dependent apoptosis pathways, including transcriptional upregulation of Puma. Moreover, our data indicate that regulation of BH3-only proteins by Akt is dispensable for Akt-dependent cell survival.

Indexed as

AnimalsApoptosisCell Growth ProcessesCytokinesHEK293 CellsHumansInterleukin-3IsoenzymesMiceMice, Inbred C57BLMice, TransgenicMyeloid CellsProto-Oncogene Proteins c-aktReceptors, Interleukin-3Signal TransductionAkt1 protein, mouseCytokinesInterleukin-3IsoenzymesProto-Oncogene Proteins c-aktReceptors, Interleukin-3

Identifiers

PMID23787999
PMCPMC3770321
OpenAlexW2041485434

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.