Evidence map›Paper›PMID 37440664›Full record

ArticleFEBS open bio2023

Selective proteasome degradation of C-terminally-truncated human WFS1 in pancreatic beta cells.

Hiraku Tokuma, Daisuke Sakano, Katsuya Tanabe, Yukio Tanizawa, Nobuaki Shiraki, Shoen Kume

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

6 authors at 2 institutions in 1 country.

Hiraku TokumaSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Daisuke SakanoSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Katsuya TanabeDivision of Endocrinology, Metabolism, Haematological Science and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, Japan.ORCID 0000-0001-9802-0584
Yukio TanizawaDivision of Endocrinology, Metabolism, Haematological Science and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Nobuaki ShirakiSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Shoen KumeSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.ORCID 0000-0002-4292-205X
Tokyo Institute of Technology · JPYamaguchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wolfram syndrome is a monogenic disease mainly caused by mutations in the WFS1 gene. Mutations in the WFS1 gene give rise to diabetes. Here, we characterized mutant WFS1 proteins by studying the stability of full-length wild-type (WT) WFS1, a missense mutant P724L, and two C-terminally truncated mutants, W837X and Y652X. We compared their stability by overexpressing them in MIN6 and HEK293T cells. The C-terminally truncated mutants W837X and Y652X are degraded more rapidly than the missense P724L mutant or wild-type WFS1 in MIN6 cells. In contrast, Y652X is more stable than WT or other mutant WFS1 proteins in HEK293T. In conclusion, we found that C-terminally truncated WFS1 mutants are selectively degraded in a cell type-specific manner.

Indexed as

Insulin-Secreting CellsWolfram SyndromeHEK293 CellsHumansMembrane ProteinsMutationProteasome Endopeptidase ComplexMembrane ProteinsProteasome Endopeptidase Complexwolframin proteinbeta cellsdegradationdiabetesendocrineproteasomeWFS1

Identifiers

PMID37440664
PMCPMC10392043
OpenAlexW4384155039

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.