Evidence map›Paper›PMID 24113187›Full record

ArticleCell death & disease2013

Gpr97 is essential for the follicular versus marginal zone B-lymphocyte fate decision.

J-J Wang, L-L Zhang, Hong-x Zhang, C-L Shen, S-y Lu, Y Kuang, Y-h Wan, W-g Wang, H-m Yan, S-y Dang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
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  8. Review
  9. Article
  10. Review
  11. Article
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Adhesion GPCRs in Kidney Development and Disease.Frontiers in cell and developmental biology · 2018
    Review
  18. Article
  19. The Adhesion G Protein-Coupled Receptor GPR97/Frontiers in immunology · 2018
    Article
  20. GαFrontiers in immunology · 2018
    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

13 authors at 2 institutions in 1 country.

J-J Wang1] State Key Laboratory of Medical Genomics, Research Center for Experimental Medicine, Rui-Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, China [2] Shanghai Research Center for Model Organisms, Shanghai, China.
L-L Zhang
Hong-x Zhang
C-L Shen
S-y Lu
Y Kuang
Y-h Wan
W-g Wang
H-m Yan
S-y Dang
J Fei
X-l Jin
Z-g Wang
Shanghai Model Organisms (China) · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gpr97 is an orphan adhesion GPCR and is highly conserved among species. Up to now, its physiological function remains largely unknown. Here, we show that Gpr97 deficiency results in an extensive reduction in B220(+) lymphocytes in mice. More intensive analyses reveal an expanded marginal zone but a decreased follicular B-cell population in Gpr97(-/-)spleen, which displays disorganized architecture characterized by diffuse, irregular B-cell areas and the absence of discrete perifollicular marginal and mantle zones. In vivo functional studies reveal that the mutant mice could generate antibody responses to T cell-dependent and independent antigens, albeit enhanced response to the former and weakened response to the latter. By screening for the molecular events involved in the observed phenotypes, we found that lambda 5 expression is downregulated and its upstream inhibitor Aiolos is increased in the spleen of mutant mice, accompanied by significantly enhanced phosphorylation and nuclear translocation of cAMP response element-binding protein. Interestingly, increased constitutive Nf-κb p50/p65 expression and activity were observed in Gpr97(-/-) spleen, implicating a crucial role of Gpr97 in regulating Nf-κb activity. These findings uncover a novel biological function of Gpr97 in regulating B-cell development, implying Gpr97 as a potential therapeutic target for treatment of immunological disorders.

Indexed as

AnimalsAnimals, NewbornB-LymphocytesBone Marrow CellsCell CountCell LineageCyclic AMP Response Element-Binding ProteinDown-RegulationGene Expression ProfilingGene TargetingImmunity, HumoralImmunoglobulin Light Chains, SurrogateImmunoglobulinsMiceMice, KnockoutNF-kappa BAdgrg3 protein, mouseCyclic AMP Response Element-Binding Proteinimmunoglobulin lambda-like polypeptide 1, mouseImmunoglobulin Light Chains, SurrogateImmunoglobulinsNF-kappa BReceptors, G-Protein-Coupled

Identifiers

PMID24113187
PMCPMC3824656
OpenAlexW1984266256

What OpenQuestion holds

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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.