Evidence map›Paper›PMID 36469690›Full record

ArticleAutophagy2023

Substitution of PINK1 Gly411 modulates substrate receptivity and turnover.

Fabienne C Fiesel, Dominika Fričová, Caleb S Hayes, Mathew A Coban, Roman Hudec, Jenny M Bredenberg, Benjamin J Broadway, Briana N Markham, Tingxiang Yan, Paige K Boneski and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A.Molecular neurodegeneration advances · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Modeling Lewy body disease withScience advances · 2024
    Article
  15. The UFMylation pathway is impaired in Alzheimer's disease.bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

25 authors at 6 institutions in 2 countries.

Fabienne C FieselDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Dominika FričováDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Caleb S HayesDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Mathew A CobanDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, USA.
Roman HudecDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Jenny M BredenbergDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Benjamin J BroadwayDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Briana N MarkhamDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Tingxiang YanDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Paige K BoneskiDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Gabriella FiorinoDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Jens O WatzlawikDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Xu HouDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Arthur M McCartyDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Laura J Lewis-TuffinCytometry and Imaging Laboratory, Department of Research, Mayo Clinic, Jacksonville, FL, USA.
Jun ZhongDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
Benjamin J MaddenProteomics Core, Medical Genome Facility, Mayo Clinic, Rochester, MN, USA.
Alban OrdureauDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA.
Heeseon AnDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA.
Andreas PuschmannDepartment of Neurology, Lund University, Skane University Hospital, Sweden.
Zbigniew K WszolekDepartment of Neurology, Mayo Clinic, Jacksonville, FL, USA.
Owen A RossDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
J Wade HarperDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA.
Thomas R CaulfieldDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Wolfdieter SpringerDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.ORCID 0000-0002-1178-3149
Mayo Clinic in Florida · USWinnMed · USHarvard University · USLund University · SEMayo Clinic · USMayo Clinic in Arizona · US

Funding

Technology and Remote Assessment CoreU19AG063911 · NIA · MAYO CLINIC ROCHESTER · PI Adam Mark Staffaroni · 2019 to 2026
$120.9M
Utilization of proteomics and lipidomics to identify modifiers of LBDU54NS110435 · NINDS · MAYO CLINIC JACKSONVILLE · PI MCLEAN, PAMELA J · 2019 to 2023
$14.5M
Molecular mechanisms of PINK1-PRKN directed mitochondrial quality controlRF1NS085070 · NINDS · MAYO CLINIC JACKSONVILLE · PI SPRINGER, WOLFDIETER · 2019 to 2019
$2.8M
Mitochondrial Sirtuin 3 in Parkinson's diseaseR01NS110085 · NINDS · MAYO CLINIC JACKSONVILLE · PI MCLEAN, PAMELA J, SPRINGER, WOLFDIETER · 2019 to 2023
$2.5M
Regulation of PINK1 and PARKIN-Dependent MitophagyR01NS083524 · NINDS · HARVARD MEDICAL SCHOOL · PI HARPER, JEFFREY W · 2020 to 2024
$2.2M
Molecular mechanisms of Parkin-directed mitochondrial quality controlR01NS085070 · NINDS · MAYO CLINIC JACKSONVILLE · PI SPRINGER, WOLFDIETER · 2014 to 2018
$1.7M
Selective autophagy in Alzheimer's disease and related dementiasR56AG062556 · NIA · MAYO CLINIC JACKSONVILLE · PI FRYER, JOHN DAVID, SPRINGER, WOLFDIETER · 2019 to 2019
$782k
NIA NIH HHS R56 AG062556NIA NIH HHS U19 AG063911NINDS NIH HHS R01 NS083524NINDS NIH HHS R01 NS085070NINDS NIH HHS R01 NS110085NINDS NIH HHS RF1 NS085070NINDS NIH HHS U54 NS110435
6 · The paper itself

Abstract

The ubiquitin (Ub) kinase-ligase pair PINK1-PRKN mediates the degradation of damaged mitochondria by macroautophagy/autophagy (mitophagy). PINK1 surveils mitochondria and upon stress accumulates on the mitochondrial surface where it phosphorylates serine 65 of Ub to activate PRKN and to drive mitochondrial turnover. While loss of either PINK1 or PRKN is genetically linked to Parkinson disease (PD) and activating the pathway seems to have great therapeutic potential, there is no formal proof that stimulation of mitophagy is always beneficial. Here we used biochemical and cell biological methods to study single nucleotide variants in the activation loop of PINK1 to modulate the enzymatic function of this kinase. Structural modeling and

Indexed as

Parkinson DiseaseProtein KinasesAutophagyHumansUbiquitinUbiquitin-Protein LigasesProtein KinasesUbiquitinUbiquitin-Protein LigasesMitophagyparkinparkinson diseasePINK1PRKNubiquitin

Identifiers

PMID36469690
PMCPMC10262784
OpenAlexW4310775732

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.