Evidence map›Paper›PMID 27776109›Full record

ArticleNature immunology2016

Sall1 is a transcriptional regulator defining microglia identity and function.

Anne Buttgereit, Iva Lelios, Xueyang Yu, Melissa Vrohlings, Natalie R Krakoski, Emmanuel L Gautier, Ryuichi Nishinakamura, Burkhard Becher, Melanie Greter

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 363 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
363citing papers in PubMed, 2 pooled it
50.5field-weighted citation impact, top 1% 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

363 citing papers in PubMed, 2 syntheses or guidelines pooled it, 576 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

303 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Anne ButtgereitInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Iva LeliosInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Xueyang YuInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Melissa VrohlingsInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Natalie R KrakoskiInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Emmanuel L GautierINSERM UMR_S 1166, Sorbonne Universités, UPMC Univ Paris 06, Pitié-Salpêtrière Hospital, Paris, France.
Ryuichi NishinakamuraDepartment of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Burkhard BecherInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-1541-7867
Melanie GreterInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
University of Zurich · CHInserm · FRKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are the resident macrophages of the central nervous system (CNS). Gene expression profiling has identified Sall1, which encodes a transcriptional regulator, as a microglial signature gene. We found that Sall1 was expressed by microglia but not by other members of the mononuclear phagocyte system or by other CNS-resident cells. Using Sall1 for microglia-specific gene targeting, we found that the cytokine receptor CSF1R was involved in the maintenance of adult microglia and that the receptor for the cytokine TGF-β suppressed activation of microglia. We then used the microglia-specific expression of Sall1 to inducibly inactivate the murine Sall1 locus in vivo, which resulted in the conversion of microglia from resting tissue macrophages into inflammatory phagocytes, leading to altered neurogenesis and disturbed tissue homeostasis. Collectively, our results show that transcriptional regulation by Sall1 maintains microglial identity and physiological properties in the CNS and allows microglia-specific manipulation in vivo.

Indexed as

AnimalsCells, CulturedGene Expression ProfilingGene SilencingHomeostasisInflammation MediatorsMacrophage ActivationMiceMice, Inbred C57BLMice, TransgenicMicrogliaNeurogenesisPhagocytesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorReceptors, Transforming Growth Factor betaTranscription FactorsCsf1r protein, mouseInflammation MediatorsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorReceptors, Transforming Growth Factor betaSall1 protein, mouseTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID27776109
OpenAlexW2537351581

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.