Evidence map›Paper›PMID 32184397›Full record

ArticleNature communications2020

Grasp55

Jiyoon Kim, Hyeyon Kim, Shin Hye Noh, Dong Geon Jang, Shi-Young Park, Dongkook Min, Hyunki Kim, Hee-Seok Kweon, Hoguen Kim, Sowon Aum and 7 more

Open access · goldAbstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Golgi defect as a major contributor to lysosomal dysfunction.Frontiers in cell and developmental biology · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Autophagy-Related Pathways in Vesicular Unconventional Protein Secretion.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Targeting the mutant p53 secretome.The Journal of clinical investigation · 2021
    Article
  18. Review
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

17 authors at 4 institutions in 1 country.

Jiyoon KimDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.ORCID http://orcid.org/0000-0002-9816-5940
Hyeyon KimDepartment of Oral Biology, BK21 PLUS, Yonsei University College of Dentistry, Yonsei-ro 50-1, Seodaemun-gu, Seoul, 03722, Korea.
Shin Hye NohDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.
Dong Geon JangDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.
Shi-Young ParkKorea Mouse Metabolic Phenotyping Center, Lee Gil Ya Cancer and Diabetes Institute, and Department of Internal Medicine, Gachon University College of Medicine, Incheon, 21999, Korea.ORCID http://orcid.org/0000-0003-2666-4289
Dongkook MinDepartment of Biochemistry and Molecular Biology, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.ORCID http://orcid.org/0000-0001-9847-6872
Hyunki KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Korea.
Hee-Seok KweonCenter for Research Equipment, Korea Basic Science Institute, Cheongju, 28119, Korea.
Hoguen KimDepartment of Pathology, Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul, 03722, Korea.ORCID http://orcid.org/0000-0002-7444-2771
Sowon AumDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.
Sookyung SeoDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.
Cheol Soo ChoiKorea Mouse Metabolic Phenotyping Center, Lee Gil Ya Cancer and Diabetes Institute, and Department of Internal Medicine, Gachon University College of Medicine, Incheon, 21999, Korea.
Hail KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Korea.ORCID http://orcid.org/0000-0002-6652-1349
Jae Woo KimDepartment of Biochemistry and Molecular Biology, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.ORCID http://orcid.org/0000-0001-5456-9495
Seok Jun MoonDepartment of Oral Biology, BK21 PLUS, Yonsei University College of Dentistry, Yonsei-ro 50-1, Seodaemun-gu, Seoul, 03722, Korea.ORCID http://orcid.org/0000-0001-7282-2888
Heon Yung GeeDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea.ORCID http://orcid.org/0000-0002-8741-6177
Min Goo LeeDepartment of Pharmacology, Brain Korea 21 Project for Medical Sciences, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, 03722, Korea. mlee@yuhs.ac.ORCID http://orcid.org/0000-0001-7436-012X
Yonsei University · KRKorea Advanced Institute of Science and Technology · KRGachon University · KRKorea Basic Science Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Golgi apparatus plays a central role in the intracellular transport of macromolecules. However, molecular mechanisms of Golgi-mediated lipid transport remain poorly understood. Here, we show that genetic inactivation of the Golgi-resident protein GRASP55 in mice reduces whole-body fat mass via impaired intestinal fat absorption and evokes resistance to high-fat diet induced body weight gain. Mechanistic analyses reveal that GRASP55 participates in the Golgi-mediated lipid droplet (LD) targeting of some LD-associated lipases, such as ATGL and MGL, which is required for sustained lipid supply for chylomicron assembly and secretion. Consequently, GRASP55 deficiency leads to reduced chylomicron secretion and abnormally large LD formation in intestinal epithelial cells upon exogenous lipid challenge. Notably, deletion of dGrasp in Drosophila causes similar defects of lipid accumulation in the midgut. These results highlight the importance of the Golgi complex in cellular lipid regulation, which is evolutionary conserved, and uncover potential therapeutic targets for obesity-associated diseases.

Indexed as

AnimalsBiological TransportDiet, High-FatDrosophilaFatsGolgi ApparatusGolgi Matrix ProteinsHumansMaleMiceMice, Inbred C57BLMice, KnockoutObesityWeight GainFatsGolgi Matrix ProteinsGorasp2 protein, mouse

Identifiers

PMID32184397
PMCPMC7078302
OpenAlexW3012300485

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.