Evidence map›Paper›PMID 30925920›Full record

ReviewMolecular cancer2019

mRNA-to-protein translation in hypoxia.

Nancy T Chee, Ines Lohse, Shaun P Brothers

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 112 citations in OpenAlex.

  1. DRP1 depletion protects NK cells from hypoxia-induced dysfunction.Redox report : communications in free radical research · 2026
    Article
  2. Article
  3. Review
  4. RiboScreenBiomedicines · 2026
    Review
  5. Enhancement of Therapeutic mRNA Translation in Cellular Stress Conditions.International journal of molecular sciences · 2026
    Review
  6. Progress and challenges in the development of advanced pancreatic cancer organoids.Journal of experimental & clinical cancer research : CR · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. FicD sensitizes cellular response to glucose fluctuations in mouse embryonic fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article

7 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

3 authors at 1 institution in 1 country.

Nancy T CheeDepartment of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, 1501 NW 10th Avenue, Miami, FL, 33136, USA.
Ines LohseDepartment of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, 1501 NW 10th Avenue, Miami, FL, 33136, USA.
Shaun P BrothersDepartment of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, 1501 NW 10th Avenue, Miami, FL, 33136, USA. spbrothers@hotmail.com.ORCID 0000-0003-2184-4037
University of Miami · US

Funding

Development of Nociceptin Receptor Agonists for Post-Traumatic Stress DisorderR01MH110441 · NIMH · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BROTHERS, SHAUN P · 2016 to 2019
$3.0M
Upregulation of Iduronidase Enzyme in MPSI DiseaseR01NS092671 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BROTHERS, SHAUN P · 2016 to 2020
$1.7M
NIMH NIH HHS R01 MH110441NINDS NIH HHS R01 NS092671
6 · The paper itself

Abstract

Cells respond to hypoxia by shifting cellular processes from general housekeeping functions to activating specialized hypoxia-response pathways. Oxygen plays an important role in generating ATP to maintain a productive rate of protein synthesis in normoxia. In hypoxia, the rate of the canonical protein synthesis pathway is significantly slowed and impaired due to limited ATP availability, necessitating an alternative mechanism to mediate protein synthesis and facilitate adaptation. Hypoxia adaptation is largely mediated by hypoxia-inducible factors (HIFs). While HIFs are well known for their transcriptional functions, they also play imperative roles in translation to mediate hypoxic protein synthesis. Such adaptations to hypoxia are often hyperactive in solid tumors, contributing to the expression of cancer hallmarks, including treatment resistance. The current literature on protein synthesis in hypoxia is reviewed here, inclusive of hypoxia-specific mRNA selection to translation termination. Current HIF targeting therapies are also discussed as are the opportunities involved with targeting hypoxia specific protein synthesis pathways.

Indexed as

Protein BiosynthesisAnimalsHumansHypoxiaNeoplasmsRNA, MessengerSignal TransductionRNA, MessengerCancerHIFHIF inhibitorsHypoxiaHypoxia-inducible factormRNA-to-protein translation

Identifiers

PMID30925920
PMCPMC6441220
OpenAlexW2943948651

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.