Evidence map›Paper›PMID 25840412›Full record

ArticleStem cell research2015

High-level Gpr56 expression is dispensable for the maintenance and function of hematopoietic stem and progenitor cells in mice.

Tata Nageswara Rao, Jonathan Marks-Bluth, Jessica Sullivan, Manoj K Gupta, Vashe Chandrakanthan, Simon R Fitch, Katrin Ottersbach, Young C Jang, Xianhua Piao, Rohit N Kulkarni and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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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

13 authors at 6 institutions in 3 countries.

Tata Nageswara RaoHoward Hughes Medical Institute, USA; Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge, MA, USA; Joslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA.
Jonathan Marks-BluthLowy Cancer Research Centre, University of New South Wales, Sydney, NSW 2052, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, NSW 2052, Australia.
Jessica SullivanHoward Hughes Medical Institute, USA; Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge, MA, USA; Joslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA.
Manoj K GuptaJoslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA.
Vashe ChandrakanthanLowy Cancer Research Centre, University of New South Wales, Sydney, NSW 2052, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, NSW 2052, Australia.
Simon R FitchDepartment of Haematology, Cambridge Institute for Medical Research University of Cambridge, Cambridge CB2 0XY, UK; Wellcome Trust - Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge CB2 0XY, UK.
Katrin OttersbachDepartment of Haematology, Cambridge Institute for Medical Research University of Cambridge, Cambridge CB2 0XY, UK; Wellcome Trust - Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge CB2 0XY, UK.
Young C JangHoward Hughes Medical Institute, USA; Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge, MA, USA; Joslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA.
Xianhua PiaoDivision of Newborn Medicine, Boston Children's Hospital, Harvard Medical School, MA, USA.
Rohit N KulkarniJoslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA.
Thomas SerwoldJoslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA.
John E PimandaLowy Cancer Research Centre, University of New South Wales, Sydney, NSW 2052, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, NSW 2052, Australia.
Amy J WagersHoward Hughes Medical Institute, USA; Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge, MA, USA; Joslin Diabetes Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02215, USA. Electronic address: amy_wagers@harvard.edu.
Harvard University · USCancer Institute of New South Wales · AUHoward Hughes Medical Institute · USJoslin Diabetes Center · USUniversity of Cambridge · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Role of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0M
Role of SerpinB1 in beta cell growthR01DK103215 · NIDDK · JOSLIN DIABETES CENTER · PI KULKARNI, ROHIT N. · 2014 to 2018
$2.6M
Aging and Rejuvenation of the hematopoietic stem cell nicheDP2OD004345 · OD · JOSLIN DIABETES CENTER · PI WAGERS, AMY JO · 2008 to 2008
$2.4M
Control of HSC proliferation and migration by the transcription factor EGR1R01HL088582 · NHLBI · JOSLIN DIABETES CENTER · PI WAGERS, AMY JO · 2009 to 2013
$2.2M
Role of IGF-1 and insulin receptors beta-cell survivalR56DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI KULKARNI, ROHIT N. · 2009 to 2010
$291k
NHLBI NIH HHS HL088582NHLBI NIH HHS R01 HL088582NIDDK NIH HHS DK103215NIDDK NIH HHS DK67536NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01 DK103215NIDDK NIH HHS R56 DK067536NIH HHS DP2 OD004345NIH HHS OD004345Wellcome Trust 97922
6 · The paper itself

Abstract

Blood formation by hematopoietic stem cells (HSCs) is regulated by a still incompletely defined network of general and HSC-specific regulators. In this study, we analyzed the role of G-protein coupled receptor 56 (Gpr56) as a candidate HSC regulator based on its differential expression in quiescent relative to proliferating HSCs and its common targeting by core HSC regulators. Detailed expression analysis revealed that Gpr56 is abundantly expressed by HSPCs during definitive hematopoiesis in the embryo and in the adult bone marrow, but its levels are reduced substantially as HSPCs differentiate. However, despite enriched expression in HSPCs, Gpr56-deficiency did not impair HSPC maintenance or function during steady-state or myeloablative stress-induced hematopoiesis. Gpr56-deficient HSCs also responded normally to physiological and pharmacological mobilization signals, despite the reported role of this GPCR as a regulator of cell adhesion and migration in neuronal cells. Moreover, Gpr56-deficient bone marrow engrafted with equivalent efficiency as wild-type HSCs in primary recipients; however, their reconstituting ability was reduced when subjected to serial transplantation. These data indicate that although GPR56 is abundantly and selectively expressed by primitive HSPCs, its high level expression is largely dispensable for steady-state and regenerative hematopoiesis.

Indexed as

AnimalsCell ProliferationFlow CytometryGene Expression ProfilingHematopoietic Stem CellsMiceReceptors, G-Protein-CoupledAdgrg1 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID25840412
PMCPMC4439311
OpenAlexW2012212570

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.