Evidence map›Paper›PMID 41718983›Full record

ReviewSub-cellular biochemistry2026

Golgi Membrane-Associated Degradation (GOMED), a New Intracellular Proteolysis Mechanism.

Shigeomi Shimizu, Shinya Honda, Satoru Torii, Satoko Arakawa, Masatsune Tsujioka, Hirofumi Yamaguchi, Hajime Tajima Sakurai

Abstract readReview
PubMed Publisher
In one paragraph

Review in Sub-cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Shigeomi ShimizuDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan. shimizu.pcb@mri.tmd.ac.jp.
Shinya HondaDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan.
Satoru ToriiDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan.
Satoko ArakawaDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan.
Masatsune TsujiokaDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan.
Hirofumi YamaguchiDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan.
Hajime Tajima SakuraiDepartment of Pathological Cell Biology, Advanced Research Initiative, Institute of Science Tokyo, Chiyoda-ku, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Golgi apparatus is a crucial organelle that is involved in various cellular processes, including cellular secretion, and is primarily responsible for the modification, sorting, and transport of proteins and lipids. However, recently, we discovered a novel Golgi function, namely, Golgi membrane-associated degradation (GOMED). GOMED is a cellular function in which the trans-Golgi membrane undergoes deformation and becomes spherical, breaking down proteins and lipids that have been internalized. This process is conserved from yeast to mammalian cells. GOMED primarily plays a role in the quality control of hormones, cytokines, and cell membrane receptors that pass through the Golgi apparatus, and is crucial for maintaining the normal function of pancreatic β cell, neurons, and intestinal epithelial cells. Therefore, abnormalities in GOMED can lead to neurodegenerative diseases and inflammatory bowel diseases.

Indexed as

Golgi ApparatusProteolysisAnimalsAutophagyHumansMembrane ProteinsNeurodegenerative DiseasesMembrane ProteinsAutophagyGolgi apparatusGOMEDULK1Wipi3

Identifiers

What OpenQuestion holds

Textmetadata
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.