Evidence map›Paper›PMID 30705402›Full record

ReviewOncogene2019

Control of mTOR signaling by ubiquitin.

Yao Jiang, Siyuan Su, Yanqiong Zhang, Jiayi Qian, Pengda Liu

Abstract readReview
In one paragraph

Review in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Defining Mechanistic Links Between the Non-Coding Variant rs17673553 inInternational journal of molecular sciences · 2025
    Article
  7. Article
  8. Article
  9. The F-box protein FBXL-5 governs vitellogenesis and lipid homeostasis inFrontiers in cell and developmental biology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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 2 institutions in 2 countries.

Yao JiangCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 430022, Wuhan, China.
Siyuan SuLineberger Comprehensive Cancer Center, Department of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Yanqiong ZhangLineberger Comprehensive Cancer Center, Department of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Jiayi QianLineberger Comprehensive Cancer Center, Department of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Pengda LiuLineberger Comprehensive Cancer Center, Department of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA. pengda_liu@med.unc.edu.
University of North Carolina at Chapel Hill · USHuazhong University of Science and Technology · CN

Funding

Elucidating a Novel Akt Activation Mechanism for Targeted Prostate Cancer TherapyR00CA181342 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, PENGDA · 2016 to 2018
$653k
NCI NIH HHS R00 CA181342
6 · The paper itself

Abstract

The evolutionarily conserved mTOR signaling pathway plays essential roles in cell growth, proliferation, metabolism and responses to cellular stresses. Hyperactivation of the mTOR signaling is observed in virtually all solid tumors and has been an attractive drug target. In addition to changes at genetic levels, aberrant activation of the mTOR signaling is also a result from dysregulated posttranslational modifications on key pathway members, such as phosphorylation that has been extensively studied. Emerging evidence also supports a critical role for ubiquitin-mediated modifications in dynamically regulating the mTOR signaling pathway, while a comprehensive review for relevant studies is missing. In this review, we will summarize characterized ubiquitination events on major mTOR signaling components, their modifying E3 ubiquitin ligases, deubiquitinases and corresponding pathophysiological functions. We will also reveal methodologies that have been used to identify E3 ligases or DUBs to facilitate the search for yet-to-be discovered ubiquitin-mediated regulatory mechanisms in mTOR signaling. We hope that our review and perspectives provide rationales and strategies to target ubiquitination for inhibiting mTOR signaling to treat human diseases.

Indexed as

AnimalsDeubiquitinating EnzymesHumansSignal TransductionTOR Serine-Threonine KinasesUbiquitinUbiquitinationUbiquitin-Protein LigasesDeubiquitinating EnzymesTOR Serine-Threonine KinasesUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID30705402
PMCPMC6621562
OpenAlexW2914176157

What OpenQuestion holds

Textmetadata
LicenceTDM
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.