Evidence map›Paper›PMID 33299977›Full record

ArticleiScience2020

Neuroplastin Modulates Anti-inflammatory Effects of MANF.

Takuya Yagi, Rie Asada, Kohsuke Kanekura, Ave Eesmaa, Maria Lindahl, Mart Saarma, Fumihiko Urano

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Neuroplastin-55 is a receptor of Manf and protects against diet-induced obesity by promoting adipose browning.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Dual role of neuroplastin in pancreatic β cells: Regulating insulin secretion and promoting islet inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 3 institutions in 3 countries.

Takuya YagiDepartment of Medicine, Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.
Rie AsadaDepartment of Medicine, Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.
Kohsuke KanekuraDepartment of Molecular Pathology, Tokyo Medical University, Tokyo 160-8402, Japan.
Ave EesmaaInstitute of Biotechnology, HiLIFE, University of Helsinki, Viikinkaari 9, 00014 Helsinki, Finland.
Maria LindahlInstitute of Biotechnology, HiLIFE, University of Helsinki, Viikinkaari 9, 00014 Helsinki, Finland.
Mart SaarmaInstitute of Biotechnology, HiLIFE, University of Helsinki, Viikinkaari 9, 00014 Helsinki, Finland.
Fumihiko UranoDepartment of Medicine, Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.
University of Helsinki · FIWashington University in St. Louis · USTokyo Medical University · JP

Funding

WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Clay F. Semenkovich · 2013 to 2026
$27.1M
ENDOPLASMIC RETICULUM IN BETA CELLSR01DK112921 · NIDDK · WASHINGTON UNIVERSITY · PI URANO, FUMIHIKO · 2017 to 2019
$1.1M
NCATS NIH HHS UL1 TR002345NIDDK NIH HHS P30 DK020579NIDDK NIH HHS R01 DK112921
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress is known to induce pro-inflammatory response and ultimately leads to cell death. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an ER-localized protein whose expression and secretion is induced by ER stress and a crucial survival factor. However, the underlying mechanism of how MANF exerts its cytoprotective activity remains unclear due to the lack of knowledge of its receptor. Here we show that Neuroplastin (NPTN) is such a receptor for MANF. Biochemical analysis shows the physiological interaction between MANF and NPTN on the cell surface. Binding of MANF to NPTN mitigates the inflammatory response and apoptosis via suppression of NF-kβ signaling. Our results demonstrate that NPTN is a cell surface receptor for MANF, which modulates inflammatory responses and cell death, and that the MANF-NPTN survival signaling described here provides potential therapeutic targets for the treatment of ER stress-related disorders, including diabetes mellitus, neurodegeneration, retinal degeneration, and Wolfram syndrome.

Indexed as

BiochemistryCell BiologyMolecular Biology

Identifiers

PMID33299977
PMCPMC7702011
OpenAlexW3099182673

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.