Evidence map›Paper›PMID 39159312›Full record

ArticleeLife2024

Iron-sulfur cluster loss in mitochondrial CISD1 mediates PINK1 loss-of-function phenotypes.

Sara Bitar, Timo Baumann, Christopher Weber, Majd Abusaada, Liliana Rojas-Charry, Patrick Ziegler, Thomas Schettgen, Isabella Eva Randerath, Vivek Venkataramani, Bernhard Michalke and 5 more

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. 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

15 authors.

Sara BitarUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.ORCID https://orcid.org/0000-0002-9369-0500
Timo BaumannUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.ORCID https://orcid.org/0000-0001-5374-380X
Christopher WeberUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.
Majd AbusaadaUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.
Liliana Rojas-CharryUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.
Patrick ZieglerInstitute for Occupational, Social and Environmental Medicine, RWTH Aachen University, Aachen, Germany.
Thomas SchettgenInstitute for Occupational, Social and Environmental Medicine, RWTH Aachen University, Aachen, Germany.ORCID https://orcid.org/0000-0003-1256-1713
Isabella Eva RanderathInstitute for Occupational, Social and Environmental Medicine, RWTH Aachen University, Aachen, Germany.
Vivek VenkataramaniComprehensive Cancer Center Mainfranken, University Hospital Würzburg, Würzburg, Germany.
Bernhard MichalkeResearch Unit Analytical BioGeoChemistry, Helmholtz Zentrum München-German, Research Center for Environmental Health GmbH, Neuherberg, Germany.
Eva-Maria HanschmannExperimental and Translational Research, Department of Otorhinolaryngology, University Hospital Essen, Essen, Germany.
Giuseppe ArenaUniversity of Luxembourg, Luxembourg Centre for Systems Biomedicine, Esch-sur-Alzette, Luxembourg.ORCID https://orcid.org/0000-0003-2398-5503
Rejko KruegerUniversity of Luxembourg, Luxembourg Centre for Systems Biomedicine, Esch-sur-Alzette, Luxembourg.
Li ZhangUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.ORCID https://orcid.org/0000-0002-6339-6087
Axel MethnerUniversity Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Mainz, Germany.ORCID https://orcid.org/0000-0002-8774-0057

Funding

Deutsche Forschungsgemeinschaft 445683311Deutsche Forschungsgemeinschaft 461705066Fonds National de la Recherche Luxembourg C21/BM/15850547/PINK1-DiaPDs
6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra of the midbrain. Familial cases of PD are often caused by mutations of PTEN-induced kinase 1 (PINK1) and the ubiquitin ligase Parkin, both pivotal in maintaining mitochondrial quality control. CISD1, a homodimeric mitochondrial iron-sulfur-binding protein, is a major target of Parkin-mediated ubiquitination. We here discovered a heightened propensity of CISD1 to form dimers in Pink1 mutant flies and in dopaminergic neurons from PINK1 mutation patients. The dimer consists of two monomers that are covalently linked by a disulfide bridge. In this conformation CISD1 cannot coordinate the iron-sulfur cofactor. Overexpressing Cisd, the

Indexed as

Drosophila ProteinsIron-Sulfur ProteinsMitochondriaAnimalsDopaminergic NeuronsDrosophila melanogasterHumansLoss of Function MutationMitochondrial ProteinsParkinson DiseasePhenotypeProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseDrosophila ProteinsIron-Sulfur ProteinsMitochondrial ProteinsPINK1 protein, DrosophilaProtein Serine-Threonine KinasesPTEN-Induced Putative Kinasecell biologyD. melanogasterdopaminergic neuronsDrosophilahumanironmitochondriamouseneuroscienceoxidative distressParkinson's disease

Identifiers

PMID39159312
PMCPMC11383524

What Socratic 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 Socratic graph.