Evidence map›Paper›PMID 36206195›Full record

ArticleBlood advances2022

GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation.

Daniel Hwang, Larissa Lumi Watanabe Ishikawa, Maryam S Seyedsadr, Elisabeth Mari, Ezgi Kasimoglu, Ziver Sahin, Alexandra Boehm, Soohwa Jang, Javad Rasouli, Courtney Vaccaro and 5 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

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  3. Distinguishing causal from tagging enhancers using single-cell multiome data.medRxiv : the preprint server for health sciences · 2026
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  10. Transcriptional regulators of fetal hemoglobin.Hematology, transfusion and cell therapy · 2024
    Review
  11. Review
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  14. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. 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

15 authors at 2 institutions in 1 country.

Daniel HwangDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.ORCID 0000-0002-6071-8271
Larissa Lumi Watanabe IshikawaDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.ORCID 0000-0003-3481-2181
Maryam S SeyedsadrDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Elisabeth MariDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Ezgi KasimogluDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Ziver SahinDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Alexandra BoehmDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.ORCID 0000-0002-9820-580X
Soohwa JangDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Javad RasouliDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.ORCID 0000-0002-0276-873X
Courtney VaccaroCenter for Applied Genomics, Leonard and Madlyn Abramson Pediatric Research Center, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Michael GonzalezCenter for Applied Genomics, Leonard and Madlyn Abramson Pediatric Research Center, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Hakon HakonarsonCenter for Applied Genomics, Leonard and Madlyn Abramson Pediatric Research Center, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Abdolmohamad RostamiDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Guang-Xian ZhangDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Bogoljub CiricDepartment of Neurology, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA.
Thomas Jefferson University · USChildren's Hospital of Philadelphia · US

Funding

Training grant on Vaccines and Immunotherapies for Infectious Diseases and CancerT32AI134646 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI SCHNELL, MATTHIAS JOHANNES, SIGAL, LUIS J · 2018 to 2022
$1.1M
NIAID NIH HHS T32 AI134646
6 · The paper itself

Abstract

GATA-binding factor 1 (GATA1) is a transcription factor that governs the development and function of multiple hematopoietic cell lineages. GATA1 is expressed in hematopoietic stem and progenitor cells (HSPCs) and is essential for erythroid lineage commitment; however, whether it plays a role in hematopoietic stem cell (HSC) biology and the development of myeloid cells, and what that role might be, remains unclear. We initially set out to test the role of eosinophils in experimental autoimmune encephalomyelitis (EAE), a model of central nervous system autoimmunity, using mice lacking a double GATA-site (ΔdblGATA), which lacks eosinophils due to the deletion of the dblGATA enhancer to Gata1, which alters its expression. ΔdblGATA mice were resistant to EAE, but not because of a lack of eosinophils, suggesting that these mice have an additional defect. ΔdblGATA mice with EAE had fewer inflammatory myeloid cells than the control mice, suggesting that resistance to EAE is caused by a defect in myeloid cells. Naïve ΔdblGATA mice also showed reduced frequency of CD11b+ myeloid cells in the blood, indicating a defect in myeloid cell production. Examination of HSPCs revealed fewer HSCs and myeloid cell progenitors in the ΔdblGATA bone marrow (BM), and competitive BM chimera experiments showed a reduced capacity of the ΔdblGATA BM to reconstitute immune cells, suggesting that reduced numbers of ΔdblGATA HSPCs cause a functional deficit during inflammation. Taken together, our data show that GATA1 regulates the number of HSPCs and that reduced GATA1 expression due to dblGATA deletion results in a diminished immune response following the inflammatory challenge.

Indexed as

GATA1 Transcription FactorHematopoietic Stem CellsNeuroinflammatory DiseasesAnimalsCell DifferentiationGene Expression RegulationMiceGata1 protein, mouseGATA1 Transcription Factor

Identifiers

PMID36206195
PMCPMC9691916
OpenAlexW4303453968

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.