Evidence map›Paper›PMID 32826333›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

LIN28B/

Xiao-Jun Li, Angelika Doetzlhofer

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. The RNA-binding protein TRIM71 is essential for hearing in humans and mice and times auditory sensory organ development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. The Reconstruction of Peripheral Auditory Circuit: Recent Advances and Future Challenges.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Analysis of miRNAs from Inner Ear Organoid-Derived Extracellular Vesicles.Journal of the Association for Research in Otolaryngology : JARO · 2025
    Article
  12. Article
  13. Article
  14. AAV-regulatedMolecular therapy. Nucleic acids · 2024
    Article
  15. Review
  16. Article
  17. Review
  18. Metabolic Profiling of Cochlear Organoids Identifies α-Ketoglutarate and NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  19. Article
  20. Auditory hair cells and spiral ganglion neurons regenerate synapses with refined release properties in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

2 authors at 1 institution in 1 country.

Xiao-Jun LiThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Angelika DoetzlhoferThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205; adoetzlhofer@jhmi.edu.ORCID 0000-0002-7424-2112
Johns Hopkins University · US

Funding

The Histology CoreP30DC005211 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI YOUNG, ERIC DANIEL · 2002 to 2016
$9.1M
Notch Signaling Pathways in Auditory Supporting Cell Differentiation and MaintenanceR01DC011571 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI DOETZLHOFER, ANGELIKA · 2011 to 2020
$3.8M
NIDCD NIH HHS P30 DC005211NIDCD NIH HHS R01 DC011571
6 · The paper itself

Abstract

Mechano-sensory hair cells within the inner ear cochlea are essential for the detection of sound. In mammals, cochlear hair cells are only produced during development and their loss, due to disease or trauma, is a leading cause of deafness. In the immature cochlea, prior to the onset of hearing, hair cell loss stimulates neighboring supporting cells to act as hair cell progenitors and produce new hair cells. However, for reasons unknown, such regenerative capacity (plasticity) is lost once supporting cells undergo maturation. Here, we demonstrate that the RNA binding protein LIN28B plays an important role in the production of hair cells by supporting cells and provide evidence that the developmental drop in supporting cell plasticity in the mammalian cochlea is, at least in part, a product of declining LIN28B-mammalian target of rapamycin (mTOR) activity. Employing murine cochlear organoid and explant cultures to model mitotic and nonmitotic mechanisms of hair cell generation, we show that loss of LIN28B function, due to its conditional deletion, or due to overexpression of the antagonistic miRNA

Indexed as

AnimalsGene Expression Regulation, DevelopmentalGenotypeHair Cells, AuditoryLabyrinth Supporting CellsMiceMicroRNAsOrganoidsRNA-Binding ProteinsTOR Serine-Threonine KinasesLin28b protein, mouseMicroRNAsmirnlet7 microRNA, mousemTOR protein, mouseRNA-Binding ProteinsTOR Serine-Threonine Kinaseshair cell regenerationinner ear cochlealet-7 miRNALIN28mTOR pathway

Identifiers

PMID32826333
PMCPMC7486708
OpenAlexW3080170780

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.