Evidence map›Paper›PMID 31964869›Full record

ArticleNature communications2020

Golgi organization is regulated by proteasomal degradation.

Avital Eisenberg-Lerner, Ron Benyair, Noa Hizkiahou, Neta Nudel, Roey Maor, Matthias P Kramer, Merav D Shmueli, Inbal Zigdon, Marina Cherniavsky Lev, Adi Ulman and 13 more

Abstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed.

  1. Article
  2. Review
  3. The pivotal role of β-lactone stereochemistry in the development of SARS-CoV-2 MProtein science : a publication of the Protein Society · 2026
    Article
  4. Review
  5. Article
  6. ORMDL Proteins Turnover via Proteasome and Autophagy Is Cell-Type Dependent and Tied to Ceramide Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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

23 authors.

Avital Eisenberg-Lerner *Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0002-0847-1355
Ron Benyair *Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Noa Hizkiahou *Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Neta NudelDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Roey MaorDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Matthias P KramerDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0002-0289-5261
Merav D ShmueliDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Inbal ZigdonDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Marina Cherniavsky LevDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Adi UlmanDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Jitka Yehudith SagivDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Molly DayanDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Bareket DassaDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Mercedes RosenwaldDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Idit ShacharDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Jie LiDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.
Yanzhuang WangDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0001-9827-4234
Nili DezorellaDepartment of Chemical Research Support, Weizmann Institute of Science, Rehovot, Israel.
Suman KhanDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0003-0564-5716
Ziv PoratFlow Cytometry Unit, Life Sciences Core Facilities, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0003-3059-181X
Eyal ShimoniDepartment of Chemical Research Support, Weizmann Institute of Science, Rehovot, Israel.
Ori AvinoamDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0003-3543-168X
Yifat MerblDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel. Yifat.merbl@weizmann.ac.il.ORCID http://orcid.org/0000-0002-3465-2221

Funding

Supplement: GOLGI BIOGENESIS AND FUNCTIONR35GM130331 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, YANZHUANG · 2019 to 2023
$2.7M
Supplement: GOLGI BIOGENESIS AND FUNCTIONR01GM112786 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, YANZHUANG · 2015 to 2019
$1.3M
Golgi-mediated Glycosylation Defects in Alzheimer’s DiseaseR56AG062225 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, YANZHUANG · 2018 to 2018
$527k
NIA NIH HHS R56 AG062225NIGMS NIH HHS R01 GM112786NIGMS NIH HHS R35 GM130331
6 · The paper itself

Abstract

The Golgi is a dynamic organelle whose correct assembly is crucial for cellular homeostasis. Perturbations in Golgi structure are associated with numerous disorders from neurodegeneration to cancer. However, whether and how dispersal of the Golgi apparatus is actively regulated under stress, and the consequences of Golgi dispersal, remain unknown. Here we demonstrate that 26S proteasomes are associated with the cytosolic surface of Golgi membranes to facilitate Golgi Apparatus-Related Degradation (GARD) and degradation of GM130 in response to Golgi stress. The degradation of GM130 is dependent on p97/VCP and 26S proteasomes, and required for Golgi dispersal. Finally, we show that perturbation of Golgi homeostasis induces cell death of multiple myeloma in vitro and in vivo, offering a therapeutic strategy for this malignancy. Taken together, this work reveals a mechanism of Golgi-localized proteasomal degradation, providing a functional link between proteostasis control and Golgi architecture, which may be critical in various secretion-related pathologies.

Indexed as

AnimalsApoptosisAutoantigensCell Line, TumorDisease Models, AnimalGolgi ApparatusHEK293 CellsHumansIntracellular MembranesIonophoresMembrane ProteinsMiceMonensinMultiple MyelomaProteasome Endopeptidase ComplexProteolysisATP dependent 26S proteaseAutoantigensGolgin subfamily A member 2IonophoresMembrane ProteinsMonensinProteasome Endopeptidase ComplexValosin Containing Protein

Identifiers

PMID31964869
PMCPMC6972958

What OpenQuestion holds

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Registered trials

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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.