Evidence map›Paper›PMID 37416455›Full record

ArticleiScience2023

Docking and stability defects in mitofusin highlight the proteasome as a potential therapeutic target.

Ira Buntenbroich, Vincent Anton, Daniel Perez-Hernandez, Tânia Simões, Felix Gaedke, Astrid Schauss, Gunnar Dittmar, Jan Riemer, Mafalda Escobar-Henriques

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Ira BuntenbroichInstitute for Genetics,University of Cologne, Cologne 50931, Germany.
Vincent AntonInstitute for Genetics,University of Cologne, Cologne 50931, Germany.
Daniel Perez-HernandezProteomics of Cellular Signaling, Luxembourg Institute of Health, Strassen 1445, Luxembourg.
Tânia SimõesInstitute for Genetics,University of Cologne, Cologne 50931, Germany.
Felix GaedkeCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne 50931, Germany.
Astrid SchaussCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne 50931, Germany.
Gunnar DittmarProteomics of Cellular Signaling, Luxembourg Institute of Health, Strassen 1445, Luxembourg.
Jan RiemerCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne 50931, Germany.
Mafalda Escobar-HenriquesInstitute for Genetics,University of Cologne, Cologne 50931, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in mitochondrial fusion are at the base of many diseases. Mitofusins power membrane-remodeling events via self-interaction and GTP hydrolysis. However, how exactly mitofusins mediate fusion of the outer membrane is still unclear. Structural studies enable tailored design of mitofusin variants, providing valuable tools to dissect this stepwise process. Here, we found that the two cysteines conserved between yeast and mammals are required for mitochondrial fusion, revealing two novel steps of the fusion cycle. C381 is dominantly required for the formation of the

Indexed as

Biological sciencesCell biologyGeneticsMolecular biology

Identifiers

PMID37416455
PMCPMC10320088

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.