Evidence map›Paper›PMID 35639700›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

GPR174 signals via G

Elise W Wolf, Zachary P Howard, Lihui Duan, Hanson Tam, Ying Xu, Jason G Cyster

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Isotype switching in human memory B cells sets intrinsic antigen-affinity thresholds that dictate antigen-driven fates.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
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  12. GPR174 signals via GProceedings of the National Academy of Sciences of the United States of America · 2022
    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

6 authors at 1 institution in 1 country.

Elise W WolfHHMI, University of California, San Francisco, CA 94143.
Zachary P HowardHHMI, University of California, San Francisco, CA 94143.
Lihui DuanHHMI, University of California, San Francisco, CA 94143.
Hanson TamHHMI, University of California, San Francisco, CA 94143.
Ying XuHHMI, University of California, San Francisco, CA 94143.
Jason G CysterHHMI, University of California, San Francisco, CA 94143.ORCID 0000-0002-4735-9745
University of California, San Francisco · US

Funding

MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
Chemokines and Lymphoid Tissue Organization and FunctionR01AI045073 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1999 to 2023
$7.6M
B LYMPHOCYTE MIGRATION AND HOMEOSTASISR01AI040098 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jason G Cyster · 1997 to 2026
$7.0M
Microbial Pathogenesis and Host DefenseT32AI060537 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joanne N. Engel · 2004 to 2026
$6.5M
Chemokines and Lymphoid Tissue Organization and FunctionR37AI045073 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jason G Cyster · 2024 to 2026
$1.7M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI040098NIAID NIH HHS R01 AI045073NIAID NIH HHS R37 AI045073NIAID NIH HHS T32 AI007334
6 · The paper itself

Abstract

GPR174 is abundantly expressed in B and T lymphocytes and has a role in restraining T cell responses, but the function of GPR174 in B cells is less clear. Here we report that upon in vitro culture B cells undergo a spontaneous GPR174-dependent activation process that is associated with marked changes in gene expression, including up-regulation of Cd86, Nr4a1, Ccr7, and phosphodiesterases. B cells lacking Gαs show a block in induction of the GPR174-dependent program. Spontaneous up-regulation of CD86 in cultured B cells is dependent on protein kinase A. Both GPR174- and Gαs-deficient B cells show enhanced survival in culture. In vivo, GPR174 contributes to NUR77 expression in follicular B cells and is needed for establishing a marginal zone compartment of normal size. Treatment of mice with lysophosphatidylserine (lysoPS), a GPR174 ligand, is sufficient to promote CD86 up-regulation by follicular B cells. These findings demonstrate that GPR174 can signal via Gαs to modulate B cell gene expression and show this can occur in vivo in response to lysoPS. Additionally, the findings illuminate a pathway that might be targeted to improve systems for the in vitro study of B cell responses.

Indexed as

B-LymphocytesImmunity, CellularReceptors, G-Protein-CoupledAnimalsB7-2 AntigenCell SurvivalGene ExpressionLigandsMiceSignal TransductionB7-2 AntigenCd86 protein, mouseGPR174 protein, mouseLigandsReceptors, G-Protein-CoupledB lymphocytesCD86GPR174G-protein–coupled receptorNUR77

Identifiers

PMID35639700
PMCPMC9191659
OpenAlexW4282935768

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.