Evidence map›Paper›PMID 39675715›Full record

ArticleThe Journal of biological chemistry2025

Dysregulation of PI4P in the trans Golgi regions activates the mammalian Golgi stress response.

Kanae Sasaki, Marika Toide, Takuya Adachi, Fumi Morishita, Yuto Watanabe, Hajime Tajima Sakurai, Sadao Wakabayashi, Satoshi Kusumi, Toshiyuki Yamaji, Kaori Sakurai and 4 more

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2025. 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. Review
  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

14 authors.

Kanae SasakiDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan. Electronic address: sasaki@sci.u-hyogo.ac.jp.
Marika ToideDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan.
Takuya AdachiDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan.
Fumi MorishitaDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan.
Yuto WatanabeDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan.
Hajime Tajima SakuraiDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan.
Sadao WakabayashiDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan.
Satoshi KusumiDivision of Morphological Sciences, Kagoshima University Graduate School of Medicine and Dental Sciences, Kagoshima, Kagoshima, Japan.
Toshiyuki YamajiDepartment of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan; Faculty of Pharmacy, Department of Microbiology and Immunology, Juntendo University, Urayasu, Chiba, Japan.
Kaori SakuraiFaculty of Engineering, Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Daisuke KogaDepartment of Microscopic Anatomy and Cell Biology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.
Kentaro HanadaDepartment of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan; Center for Quality Management Systems, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan.
Masafumi YohdaFaculty of Engineering, Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Hiderou YoshidaDepartment of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan. Electronic address: hide@sci.u-hyogo.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Golgi stress response is an important cytoprotective system that enhances Golgi function in response to cellular demand, while cells damaged by prolonged Golgi stress undergo cell death. OSW-1, a natural compound with anticancer activity, potently inhibits OSBP that transports cholesterol and phosphatidylinositol-4-phosphate (PI4P) at contact sites between the endoplasmic reticulum and the Golgi apparatus. Previously, we reported that OSW-1 induces the Golgi stress response, resulting in Golgi stress-induced transcription and cell death. However, the underlying molecular mechanism has been unknown. To reveal the mechanism of a novel pathway of the Golgi stress response regulating transcriptional induction and cell death (the PI4P pathway), we performed a genome-wide KO screen and found that transcriptional induction as well as cell death induced by OSW-1 was repressed by the loss of regulators of PI4P synthesis, such as PITPNB and PI4KB. Our data indicate that OSW-1 induces Golgi stress-dependent transcriptional induction and cell death through dysregulation of the PI4P metabolism in the Golgi.

Indexed as

Golgi ApparatusPhosphatidylinositol PhosphatesStress, PhysiologicalCell DeathHeLa CellsHumansphosphatidylinositol 4-phosphatePhosphatidylinositol PhosphatescancerGolgi stress responseOSW-1phosphatidylinositol-4-phosphatethe genome-wide CRISPR-Cas9 KO screening

Identifiers

PMID39675715
PMCPMC11770552

What Socratic 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 Socratic graph.