Evidence map›Paper›PMID 30340324›Full record

ReviewInternational journal of molecular sciences2018

Unfolded Protein Response-Dependent Communication and Contact among Endoplasmic Reticulum, Mitochondria, and Plasma Membrane.

Atsushi Saito, Kazunori Imaizumi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 61 citations in OpenAlex.

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  8. Non-canonical activation of IRE1α duringbioRxiv : the preprint server for biology · 2024
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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

2 authors at 1 institution in 1 country.

Atsushi SaitoDepartment of Stress Protein Processing, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. saitoa@hiroshima-u.ac.jp.
Kazunori ImaizumiDepartment of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. imaizumi@hiroshima-u.ac.jp.
Hiroshima University · JP

Funding

Japan Society for the Promotion of Science JP17H06416, JP17H01424
6 · The paper itself

Abstract

The function of the endoplasmic reticulum (ER) can be impaired by changes to the extra- and intracellular environment, such as disruption of calcium homeostasis, expression of mutated proteins, and oxidative stress. In response to disruptions to ER homeostasis, eukaryotic cells activate canonical branches of signal transduction cascades, collectively termed the unfolded protein response (UPR). The UPR functions to remove or recover the activity of misfolded proteins that accumulated in the ER and to avoid irreversible cellular damage. Additionally, the UPR plays unique physiological roles in the regulation of diverse cellular events, including cell differentiation and development and lipid biosynthesis. Recent studies have shown that these important cellular events are also regulated by contact and communication among organelles. These reports suggest strong involvement among the UPR, organelle communication, and regulation of cellular homeostasis. However, the precise mechanisms for the formation of contact sites and the regulation of ER dynamics by the UPR remain unresolved. In this review, we summarize the current understanding of how the UPR regulates morphological changes to the ER and the formation of contact sites between the ER and other organelles. We also review how UPR-dependent connections between the ER and other organelles affect cellular and physiological functions.

Indexed as

Signal TransductionUnfolded Protein ResponseAnimalsCell MembraneEndoplasmic ReticulumEndoplasmic Reticulum StressHumansIntracellular MembranesMitochondriaProtein Processing, Post-TranslationalProtein TransportER morphologyER-PM contact sitesmitochondria-associated ER membraneunfolded protein response

Identifiers

PMID30340324
PMCPMC6213962
OpenAlexW2894384976

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.