Evidence map›Paper›PMID 25327638›Full record

ReviewCell proliferation2014

UNC51-like kinase 1, autophagic regulator and cancer therapeutic target.

Y Chen, J He, M Tian, S-Y Zhang, M-R Guo, R Kasimu, J-H Wang, L Ouyang

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell proliferation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Dialogue between programmed cell death and psoriasis.Postepy dermatologii i alergologii · 2025
    Review
  3. Article
  4. Article
  5. Programmed Cell Death in Diabetic Nephropathy: A Review of Apoptosis, Autophagy, and Necroptosis.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Review
  6. Review
  7. Effect of moxibustion on autophagy and the inflammatory response of synovial cells in rheumatoid arthritis model rat.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022
    Article
  8. Review
  9. Investigation the Role of Autophagy in Non-Small Cell Lung Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021
    Article
  10. Mechanisms of TLR4-Mediated Autophagy and Nitroxidative Stress.Frontiers in cellular and infection microbiology · 2021
    Review
  11. Review
  12. The Messenger Apps of the cell: Extracellular Vesicles as Regulatory Messengers of Microglial Function in the CNS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
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

8 authors at 3 institutions in 1 country.

Y ChenState Key Laboratory of Biotherapy & Collaborative Innovation Center of Biotherapy, Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
J He
M Tian
S-Y Zhang
M-R Guo
R Kasimu
J-H Wang
L Ouyang
Sichuan University · CNState Key Laboratory of BiotherapyXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, the cell process of self-digestion, plays a pivotal role in maintaining energy homoeostasis and protein synthesis. When required, it causes degradation of long-lived proteins and damaged organelles, indicating that it may play a dual role in cancer, by both protecting against and promoting cell death. The autophagy-related gene (Atg) family, with more than 35 members, regulates multiple stages of the process. Serine/threonine protein kinase Atg1 in yeast, for example, can interact with other ATG gene products, functioning in autophagosome formation. One mammalian homologue of Atg1, UNC-51-like kinase 1 (ULK1) and its related complex ULK1-mAtg13-FIP200 can mediate autophagy under nutrient-deprived conditions, by protein-protein interactions and post-translational modifications. Although specific mechanisms of how ULK1 and its complex transduces upstream signals to the downstream central autophagy pathways is not fully understood, past studies have indicated that ULK1 can both suppress and promote tumour growth under different conditions. Here, we summarize some properties of ULK1 which can regulate autophagy in cancer, which may shed new light on future cancer therapy strategies, utilizing ULK1 as a potential new target.

Indexed as

AutophagyAnimalsAutophagy-Related Protein-1 HomologHumansIntracellular Signaling Peptides and ProteinsMicroRNAsNeoplasmsProtein Serine-Threonine KinasesTOR Serine-Threonine KinasesAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsMicroRNAsProtein Serine-Threonine KinasesTOR Serine-Threonine KinasesULK1 protein, human

Identifiers

PMID25327638
PMCPMC6495397
OpenAlexW2011670301

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.