Evidence map›Paper›PMID 31376929›Full record

ReviewTrends in genetics : TIG2019

Ribosomopathies: Old Concepts, New Controversies.

Katherine I Farley-Barnes, Lisa M Ogawa, Susan J Baserga

Abstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing 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.

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

132 citing papers in PubMed.

  1. Review
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  16. Fibrillarin: bridging ribosome biogenesis and apoptosis in cellular stress and disease.Apoptosis : an international journal on programmed cell death · 2026
    Review
  17. Systematic analysis of noncanonical ribosomal protein paralogs does not provide evidence for specialized functions inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Article
  19. Article
  20. Article

72 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.

Katherine I Farley-BarnesDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA.
Lisa M OgawaDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA.
Susan J BasergaDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: susan.baserga@yale.edu.

Funding

Skill Development for Diverse Scientific Careers: A New Course Predoctoral Program in Cellular and Molecular BiologyT32GM007223 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 1985 to 2019
$31.0M
Novel regulatory networks driving human ribosome biogenesisR35GM131687 · NIGMS · YALE UNIVERSITY · PI Susan J Baserga · 2019 to 2026
$5.1M
Key factors in human ribosome biogenesisR01GM115710 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 2015 to 2018
$1.6M
A New Role for the PAX9 Protein in Ribosome BiogenesisR01GM122926 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 2017 to 2019
$663k
The intersection of Alzheimer’s disease and ribosome biogenesis through Amyloid Beta Precursor Protein Binding Family B Member 1 (APBB1; FE65)F31AG058405 · NIA · YALE UNIVERSITY · PI MCLEAN, LISA OGAWA · 2017 to 2020
$128k
PAX9, ribosome biogenesis, and congenital diseaseF31DE026946 · NIDCR · YALE UNIVERSITY · PI FARLEY, KATHERINE IRENE · 2017 to 2019
$81k
NIA NIH HHS F31 AG058405NIDCR NIH HHS F31 DE026946NIGMS NIH HHS R01 GM115710NIGMS NIH HHS R01 GM122926NIGMS NIH HHS R35 GM131687NIGMS NIH HHS T32 GM007223
6 · The paper itself

Abstract

Ribosomopathies are a diverse subset of diseases caused by reduced expression of, or mutations in, factors necessary for making ribosomes, the protein translation machinery in the cell. Despite the ubiquitous need for ribosomes in all cell types, ribosomopathies manifest with tissue-specific defects and sometimes increased cancer susceptibility, but few treatments target the underlying cause. By highlighting new research in the field, we review current hypotheses for the basis of this tissue specificity. Based on new work, we broaden our understanding of the role of ribosome biogenesis in diverse tissue types throughout embryonic development. We also pose the question of whether previously described human conditions such as aging can be at least partially attributed to defects in making ribosomes.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseRNA, RibosomalAnimalsHumansMultigene FamilyRNA PrecursorsRNA Processing, Post-TranscriptionalTranscription, GeneticRNA PrecursorsRNA, Ribosomalagingcancerneurodegenerationribosome concentration hypothesisribosomopathyspecialized ribosome

Identifiers

PMID31376929
PMCPMC6852887

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.