Evidence map›Paper›PMID 32452062›Full record

ArticleThe EMBO journal2020

A splicing isoform of GPR56 mediates microglial synaptic refinement via phosphatidylserine binding.

Tao Li, Brian Chiou, Casey K Gilman, Rong Luo, Tatsuhiro Koshi, Diankun Yu, Hayeon C Oak, Stefanie Giera, Erin Johnson-Venkatesh, Allie K Muthukumar and 3 more

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

109 citing papers in PubMed, 166 citations in OpenAlex.

  1. Review
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  4. Review
  5. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  6. Article
  7. Article
  8. Review
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  13. Roles of Glia in Synapse Nano-organization.Advances in neurobiology · 2026
    Review
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  15. Review
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  17. Article
  18. The far extracellular CUB domain of the adhesion GPCR ADGRG6/GPR126 is a key regulator of receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Tao LiEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco (UCSF), San Francisco, CA, USA.ORCID 0000-0002-9174-1271
Brian ChiouEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco (UCSF), San Francisco, CA, USA.
Casey K GilmanDepartment of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Rong LuoDepartment of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Tatsuhiro KoshiDepartment of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Diankun YuEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco (UCSF), San Francisco, CA, USA.
Hayeon C OakEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco (UCSF), San Francisco, CA, USA.
Stefanie GieraDepartment of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Erin Johnson-VenkateshF. M. Kirby Neurobiology Center, Children's Hospital, Harvard Medical School, Boston, MA, USA.
Allie K MuthukumarF. M. Kirby Neurobiology Center, Children's Hospital, Harvard Medical School, Boston, MA, USA.
Beth StevensF. M. Kirby Neurobiology Center, Children's Hospital, Harvard Medical School, Boston, MA, USA.
Hisashi UmemoriF. M. Kirby Neurobiology Center, Children's Hospital, Harvard Medical School, Boston, MA, USA.
Xianhua PiaoEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco (UCSF), San Francisco, CA, USA.ORCID 0000-0001-7540-6767
Boston Children's Hospital · USUniversity of California, San Francisco · US

Funding

How do neurons in the brain decide to refine their synaptic connections in vivo?R01MH111647 · NIMH · BOSTON CHILDREN'S HOSPITAL · PI Chinfei Chen, Hisashi Umemori · 2017 to 2026
$6.8M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2M
Adhesion G Protein-Coupled Receptors in CNS Development and RegenerationR01NS094164 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PIAO, XIANHUA · 2015 to 2025
$4.5M
Investigating CD47-SIRPa as novel protective signals during CNS synaptic pruningR01NS092578 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI STEVENS, BETH ANN, UMEMORI, HISASHI · 2015 to 2019
$2.9M
Glial Mechanisms Of Developmental Synapse RefinementR01NS108446 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PIAO, XIANHUA · 2018 to 2022
$2.9M
Adhesion GPCR interactome landscaping by in vivo biotinylation proteomicsR21NS108312 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PIAO, XIANHUA · 2018 to 2019
$448k
NICHD NIH HHS U54 HD090255NIMH NIH HHS R01 MH111647NINDS NIH HHS R01 NS092578NINDS NIH HHS R01 NS094164NINDS NIH HHS R01 NS108446NINDS NIH HHS R21 NS108312
6 · The paper itself

Abstract

Developmental synaptic remodeling is important for the formation of precise neural circuitry, and its disruption has been linked to neurodevelopmental disorders such as autism and schizophrenia. Microglia prune synapses, but integration of this synapse pruning with overlapping and concurrent neurodevelopmental processes, remains elusive. Adhesion G protein-coupled receptor ADGRG1/GPR56 controls multiple aspects of brain development in a cell type-specific manner: In neural progenitor cells, GPR56 regulates cortical lamination, whereas in oligodendrocyte progenitor cells, GPR56 controls developmental myelination and myelin repair. Here, we show that microglial GPR56 maintains appropriate synaptic numbers in several brain regions in a time- and circuit-dependent fashion. Phosphatidylserine (PS) on presynaptic elements binds GPR56 in a domain-specific manner, and microglia-specific deletion of Gpr56 leads to increased synapses as a result of reduced microglial engulfment of PS

Indexed as

Alternative SplicingAnimalsMiceMice, TransgenicMicrogliaPhosphatidylserinesProtein BindingProtein IsoformsReceptors, G-Protein-CoupledSynapsesAdgrg1 protein, mousePhosphatidylserinesProtein IsoformsReceptors, G-Protein-Coupledadhesion GPCRGPR56microgliaphosphatidylserinesynaptic pruning

Identifiers

PMID32452062
PMCPMC7429740
OpenAlexW3032487381

What OpenQuestion holds

Textmetadata
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.