Evidence map›Paper›PMID 33372036›Full record

ArticleThe Journal of biological chemistry

The ATPase mechanism of myosin 15, the molecular motor mutated in DFNB3 human deafness.

Fangfang Jiang, Yasuharu Takagi, Arik Shams, Sarah M Heissler, Thomas B Friedman, James R Sellers, Jonathan E Bird

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Expression, Purification, and In Vitro Analysis of Myosin.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Unconventional Myosins fromBiomolecules · 2022
    Review
  9. Myosin motors in sensory hair bundle assembly.Current opinion in cell biology · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Functional Role of Class III Myosins in Hair Cells.Frontiers in cell and developmental biology · 2021
    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

7 authors at 3 institutions in 1 country.

Fangfang JiangDepartment of Pharmacology and Therapeutics, and the Myology Institute, University of Florida College of Medicine, Gainesville, Florida, USA.
Yasuharu TakagiLaboratory of Molecular Physiology, Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Arik ShamsLaboratory of Molecular Genetics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland, USA.
Sarah M HeisslerDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Thomas B FriedmanLaboratory of Molecular Genetics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland, USA.
James R SellersLaboratory of Molecular Physiology, Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Jonathan E BirdDepartment of Pharmacology and Therapeutics, and the Myology Institute, University of Florida College of Medicine, Gainesville, Florida, USA. Electronic address: j.bird@ufl.edu.
National Institutes of Health · USUniversity of Florida · USThe Ohio State University Wexner Medical Center · US

Funding

Identification of Genes Causing Syndromic And Nonsyndromic Hearing ImpairmentZIADC000039 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI FRIEDMAN, THOMAS · 2009 to 2025
$48.7M
Expression Studies of Other Unconventional MyosinsZIAHL004232 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SELLERS, JAMES · 2009 to 2025
$11.7M
Molecular Mechanisms of Hair Bundle Development and MaintenanceR01DC018827 · NIDCD · UNIVERSITY OF FLORIDA · PI Jonathan Edward Bird · 2020 to 2026
$3.0M
Myosin XVA and Other Genes Essential for Stereocilia MorphogenesisZ01DC000048 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI FRIEDMAN, THOMAS BAER · 1998 to 2008
$1.7M
Intramural NIH HHS Z01 DC000048NIDCD NIH HHS R01 DC018827
6 · The paper itself

Abstract

Cochlear hair cells each possess an exquisite bundle of actin-based stereocilia that detect sound. Unconventional myosin 15 (MYO15) traffics and delivers critical molecules required for stereocilia development and thus is essential for building the mechanosensory hair bundle. Mutations in the human MYO15A gene interfere with stereocilia trafficking and cause hereditary hearing loss, DFNB3, but the impact of these mutations is not known, as MYO15 itself is poorly characterized. To learn more, we performed a kinetic study of the ATPase motor domain to characterize its mechanochemical cycle. Using the baculovirus-Sf9 system, we purified a recombinant minimal motor domain (S1) by coexpressing the mouse MYO15 ATPase, essential and regulatory light chains that bind its IQ domains, and UNC45 and HSP90A chaperones required for correct folding of the ATPase. MYO15 purified with either UNC45A or UNC45B coexpression had similar ATPase activities (k

Indexed as

Adenosine TriphosphatasesAnimalsDeafnessHair Cells, AuditoryHearingHumansKineticsMiceMolecular ChaperonesMutationMyosinsProtein DomainsStereociliaAdenosine TriphosphatasesMolecular ChaperonesMYO15A protein, humanMyosinsUnc45 protein, mouseactinATPasecytoskeletonhair cellhearingmyosin

Identifiers

PMID33372036
PMCPMC7948958
OpenAlexW3115892413

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.