Evidence map›Paper›PMID 33560396›Full record

ArticleBlood advances2021

Unexpected redundancy of Gpr56 and Gpr97 during hematopoietic cell development and differentiation.

Antonio Maglitto, Samanta A Mariani, Emma de Pater, Carmen Rodriguez-Seoane, Chris S Vink, Xianhua Piao, Mari-Liis Lukke, Elaine Dzierzak

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  2. Gpr171 regulates embryonic hematopoietic stem cell emergence via ERK1/2 and Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  7. Review
  8. Zebrafish: a convenient tool for myelopoiesis research.Cell regeneration (London, England) · 2023
    Review
  9. Article
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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

8 authors at 3 institutions in 3 countries.

Antonio MaglittoCentre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Samanta A MarianiCentre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Emma de PaterDepartment of Hematology, Erasmus Medical Center, Rotterdam, The Netherlands; and.
Carmen Rodriguez-SeoaneCentre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Chris S VinkCentre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Xianhua PiaoNewborn Brain Research Institute, Department of Pediatrics, University of California San Francisco, San Francisco, CA.
Mari-Liis LukkeCentre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Elaine DzierzakCentre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Centre for Inflammation Research · GBErasmus MC · NLUniversity of California, San Francisco · US

Funding

Characterization of the first HSCs during mouse ontogenyR37DK054077 · NIDDK · UNIVERSITY OF EDINBURGH · PI DZIERZAK, ELAINE A · 2006 to 2015
$2.7M
NIDDK NIH HHS R37 DK054077
6 · The paper itself

Abstract

Integrated molecular signals regulate cell fate decisions in the embryonic aortic endothelium to drive hematopoietic stem cell (HSC) generation during development. The G-protein-coupled receptor 56 (Gpr56, also called Adgrg1) is the most highly upregulated receptor gene in cells that take on hematopoietic fate and is expressed by adult bone marrow HSCs. Despite the requirement for Gpr56 in hematopoietic stem/progenitor cell (HS/PC) generation in zebrafish embryos and the highly upregulated expression of GPR56 in treatment-resistant leukemic patients, its function in normal mammalian hematopoiesis remains unclear. Here, we examine the role of Gpr56 in HS/PC development in Gpr56 conditional knockout (cKO) mouse embryos and Gpr knockout (KO) embryonic stem cell (ESC) hematopoietic differentiation cultures. Our results show a bias toward myeloid differentiation of Gpr56 cKO fetal liver HSCs and an increased definitive myeloid progenitor cell frequency in Gpr56KO ESC differentiation cultures. Surprisingly, we find that mouse Gpr97 can rescue Gpr56 morphant zebrafish hematopoietic generation, and that Gpr97 expression is upregulated in mouse Gpr56 deletion models. When both Gpr56 and Gpr97 are deleted in ESCs, no or few hematopoietic PCs (HPCs) are generated upon ESC differentiation. Together, our results reveal novel and redundant functions for these 2 G-protein coupled receptors in normal mammalian hematopoietic cell development and differentiation.

Indexed as

Hematopoietic Stem Cell TransplantationZebrafishAnimalsCell DifferentiationHematopoiesisHematopoietic Stem CellsHumansMiceReceptors, G-Protein-CoupledAdgrg1 protein, mouseAdgrg3 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID33560396
PMCPMC7876891
OpenAlexW3127842669

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.