Evidence map›Paper›PMID 28431241›Full record

ReviewCell2017

AKT/PKB Signaling: Navigating the Network.

Brendan D Manning, Alex Toker

Registry-linked trialAbstract readReview
In one paragraph

Review in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05563831 (Evaluation Nationale Des Enfants et Adultes Avec Syndromes d'Hypercroissance Dysharmonieuse National Evaluation of Patients With PIK3CA-Related Overgrowth Spectrum), which is not on this map. Cited by 2,170 papers.

0numbers the graph read from it
0cells of the map it votes in
2,170citing papers in PubMed
–field-weighted citation impact
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.

NCT05563831 completednot on this mapstarted 2023, after this paper: background citation

Evaluation Nationale Des Enfants et Adultes Avec Syndromes d'Hypercroissance Dysharmonieuse National Evaluation of Patients With PIK3CA-Related Overgrowth Spectrum (PROS)

TypeobservationalSponsorInstitut National de la Santé Et de la Recherche Médicale, FranceRan2023 to 2023Enrolled28ConditionsPIK3CA-related Overgrowth Spectrum, CLOVES Syndrome, Klippel Trenaunay Syndrome, MegalencephalyArmsnational registry
3 · Its place in the literature

Who cites it

2,170 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. AKT Phosphorylation of FOXK2 at Ser398 Impacts Breast Cancer Cell Growth and Viability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Glycolysis Drives TLR Ligand-Induced Maturation and Immune Activation of Liver Sinusoidal Endothelial Cells.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

2,110 more citing papers are in PubMed but not listed here.

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

2 authors.

Brendan D ManningDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. Electronic address: bmanning@hsph.harvard.edu.
Alex TokerDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, and Ludwig Center at Harvard, Boston, MA 02215, USA. Electronic address: atoker@bidmc.harvard.edu.

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Decoding and Targeting the PI3K-mTOR Signaling Network in CancerR35CA197459 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI BRENDAN D. MANNING · 2015 to 2026
$10.8M
Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
Exploiting Metabolic Vulnerabilities in the PI3K and Akt Pathway in Cancer for Therapeutic BenefitR01CA200671 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TOKER, ALEX · 2016 to 2020
$2.0M
NCI NIH HHS P01 CA120964NCI NIH HHS R01 CA177910NCI NIH HHS R01 CA200671NCI NIH HHS R35 CA197459
6 · The paper itself

Abstract

The Ser and Thr kinase AKT, also known as protein kinase B (PKB), was discovered 25 years ago and has been the focus of tens of thousands of studies in diverse fields of biology and medicine. There have been many advances in our knowledge of the upstream regulatory inputs into AKT, key multifunctional downstream signaling nodes (GSK3, FoxO, mTORC1), which greatly expand the functional repertoire of AKT, and the complex circuitry of this dynamically branching and looping signaling network that is ubiquitous to nearly every cell in our body. Mouse and human genetic studies have also revealed physiological roles for the AKT network in nearly every organ system. Our comprehension of AKT regulation and functions is particularly important given the consequences of AKT dysfunction in diverse pathological settings, including developmental and overgrowth syndromes, cancer, cardiovascular disease, insulin resistance and type 2 diabetes, inflammatory and autoimmune disorders, and neurological disorders. There has also been much progress in developing AKT-selective small molecule inhibitors. Improved understanding of the molecular wiring of the AKT signaling network continues to make an impact that cuts across most disciplines of the biomedical sciences.

Indexed as

Signal TransductionAnimalsDrug TherapyHumansIsoenzymesMolecular Targeted TherapyPhosphorylationProto-Oncogene Proteins c-aktIsoenzymesProto-Oncogene Proteins c-akt

Identifiers

PMID28431241
PMCPMC5546324

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.