Evidence map›Paper›PMID 40047103›Full record

ReviewTraffic (Copenhagen, Denmark)

Disease-Associated Factors at the Endoplasmic Reticulum-Golgi Interface.

Miharu Maeda, Masashi Arakawa, Kota Saito

Abstract readReview
In one paragraph

Review in Traffic (Copenhagen, Denmark). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

3 authors.

Miharu MaedaDepartment of Biological Informatics and Experimental Therapeutics, Graduate School of Medicine, Akita University, Akita, Japan.ORCID 0000-0002-5573-2167
Masashi ArakawaDepartment of Biological Informatics and Experimental Therapeutics, Graduate School of Medicine, Akita University, Akita, Japan.ORCID 0009-0001-3759-7272
Kota SaitoDepartment of Biological Informatics and Experimental Therapeutics, Graduate School of Medicine, Akita University, Akita, Japan.ORCID 0000-0003-2478-2687

Funding

Asahi Glass FoundationJapan Society for the Promotion of Science 23K24023Japan Society for the Promotion of Science 23K27123Japan Society for the Promotion of Science 24K18067Japan Society for the Promotion of Science 24K22065Naito FoundationPrincess Takamatsu Cancer Research FoundationTakeda Science Foundation
6 · The paper itself

Abstract

The endoplasmic reticulum (ER)-Golgi interface is essential for directing the transport of proteins synthesized in the ER to the Golgi apparatus via the ER-Golgi intermediate compartment, as well as for recycling proteins back to the ER. This transport is facilitated by various components, including COPI and COPII coat protein complexes and the transport protein particle complex. Recently, the ER-Golgi transport pathway has gained attention due to emerging evidence of nonvesicular transport mechanisms and the regulation of trafficking through liquid-liquid phase separation. Numerous diseases have been linked to mutations in proteins localized at the ER-Golgi interface, highlighting the need for comprehensive analysis of these conditions. This review examines the disease phenotypes associated with dysfunctional ER-Golgi transport factors and explores their cellular effects, providing insights into potential therapeutic strategies.

Indexed as

Endoplasmic ReticulumGolgi ApparatusAnimalsCOP-Coated VesiclesHumansProtein TransportCOPICOPIIdisease‐associated factorendoplasmic reticulumER exit siteERGICGolgiliquid‐phase separationnonvesicular transportTRAPP complex

Identifiers

PMID40047103
PMCPMC11883524

What OpenQuestion holds

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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.