Evidence map›Paper›PMID 27308346›Full record

ReviewMolecular & cellular oncology

Impact of acetylation on tumor metabolism.

Di Zhao, Fu-Long Li, Zhou-Li Cheng, Qun-Ying Lei

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Mitochondria in cancer.Cell stress · 2020
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

4 authors at 2 institutions in 2 countries.

Di ZhaoKey Laboratory of Molecular Medicine; Ministry of Education, and Department of Biochemistry and Molecular Biology; Fudan University Shanghai Medical College; Shanghai, People's Republic of China; Molecular and Cell Biology Lab; Institutes of Biomedical Sciences; Fudan University; Shanghai, People's Republic of China.
Fu-Long LiKey Laboratory of Molecular Medicine; Ministry of Education, and Department of Biochemistry and Molecular Biology; Fudan University Shanghai Medical College; Shanghai, People's Republic of China; Molecular and Cell Biology Lab; Institutes of Biomedical Sciences; Fudan University; Shanghai, People's Republic of China.
Zhou-Li ChengKey Laboratory of Molecular Medicine; Ministry of Education, and Department of Biochemistry and Molecular Biology; Fudan University Shanghai Medical College; Shanghai, People's Republic of China; Molecular and Cell Biology Lab; Institutes of Biomedical Sciences; Fudan University; Shanghai, People's Republic of China.
Qun-Ying LeiKey Laboratory of Molecular Medicine; Ministry of Education, and Department of Biochemistry and Molecular Biology; Fudan University Shanghai Medical College; Shanghai, People's Republic of China; Molecular and Cell Biology Lab; Institutes of Biomedical Sciences; Fudan University; Shanghai, People's Republic of China.
Fudan University · CNInstitute of Molecular and Cell Biology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetylation of protein lysine residues is a reversible and dynamic process that is controlled by histone acetyltransferases (HATs) and deacetylases (HDACs and SIRTs). Recent studies have revealed that acetylation modulates not only nuclear proteins but also cytoplasmic or mitochondrial proteins, including many metabolic enzymes. In tumors, cellular metabolism is reprogrammed to provide intermediates for biosynthesis such as nucleotides, fatty acids, and amino acids, and thereby favor the rapid proliferation of cancer cells and tumor development. An increasing number of investigations have indicated that acetylation plays an important role in tumor metabolism. Here, we summarize the substrates that are modified by acetylation, especially oncogenes, tumor suppressor genes, and enzymes that are implicated in tumor metabolism.

Indexed as

acetylationmetabolic enzymeoncogenetumor metabolismtumor suppressor

Identifiers

PMID27308346
PMCPMC4905055
OpenAlexW2044897645

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.