Evidence map›Paper›PMID 25220463›Full record

ArticleCell reports2014

The phosphate exporter xpr1b is required for differentiation of tissue-resident macrophages.

Ana M Meireles, Celia E Shiau, Catherine A Guenther, Harwin Sidik, David M Kingsley, William S Talbot

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. XPR1: a regulator of cellular phosphate homeostasis rather than a Pi exporter.Pflugers Archiv : European journal of physiology · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Functional macrophages and gastrointestinal disorders.World journal of gastroenterology · 2018
    Review
  19. Article
  20. HG3 (Bethesda, Md.) · 2017
    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 2 institutions in 1 country.

Ana M MeirelesDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Celia E ShiauDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Catherine A GuentherDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Harwin SidikDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
David M KingsleyDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
William S TalbotDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: william.talbot@stanford.edu.
Stanford University · USHoward Hughes Medical Institute · US

Funding

Genetic Control of Microglia and Neural MacrophagesR01NS065787 · NINDS · STANFORD UNIVERSITY · PI TALBOT, WILLIAM S · 2009 to 2013
$1.7M
Genetic dissection of the role of macrophages in axonal myelination in zebrafishF32NS067754 · NINDS · STANFORD UNIVERSITY · PI SHIAU, CELIA E · 2010 to 2012
$153k
Howard Hughes Medical InstituteNINDS NIH HHS 5F32NS067754NINDS NIH HHS F32 NS067754NINDS NIH HHS R01 NS065787
6 · The paper itself

Abstract

Phosphate concentration is tightly regulated at the cellular and organismal levels. The first metazoan phosphate exporter, XPR1, was recently identified, but its in vivo function remains unknown. In a genetic screen, we identified a mutation in a zebrafish ortholog of human XPR1, xpr1b. xpr1b mutants lack microglia, the specialized macrophages that reside in the brain, and also displayed an osteopetrotic phenotype characteristic of defects in osteoclast function. Transgenic expression studies indicated that xpr1b acts autonomously in developing macrophages. xpr1b mutants display no gross developmental defects that may arise from phosphate imbalance. We constructed a targeted mutation of xpr1a, a duplicate of xpr1b in the zebrafish genome, to determine whether Xpr1a and Xpr1b have redundant functions. Single mutants for xpr1a were viable, and double mutants for xpr1b;xpr1a were similar to xpr1b single mutants. Our genetic analysis reveals a specific role for the phosphate exporter Xpr1 in the differentiation of tissue macrophages.

Indexed as

Cell DifferentiationAnimalsAnimals, Genetically ModifiedBone DevelopmentBone RemodelingBrainEmbryo, NonmammalianHumansMacrophagesMicrogliaMutationPhenotypePhosphatesProtein IsoformsReceptors, G-Protein-CoupledReceptors, VirusPhosphatesProtein IsoformsReceptors, G-Protein-CoupledReceptors, VirusXenotropic and Polytropic Retrovirus ReceptorXPR1 protein, humanZebrafish Proteins

Identifiers

PMID25220463
PMCPMC4177277
OpenAlexW2047154766

What OpenQuestion holds

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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.