Evidence map›Paper›PMID 30858552›Full record

ArticleLeukemia2019

Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice.

Lin Han, Vikas Madan, Anand Mayakonda, Pushkar Dakle, Teoh Weoi Woon, Pavithra Shyamsunder, Hazimah Binte Mohd Nordin, Zeya Cao, Janani Sundaresan, Ienglam Lei and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. BRD9 at the crossroads of splicing, chromatin remodeling, and hematopoiesis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Chromatin remodeling in tissue stem cell fate determination.Cell regeneration (London, England) · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 3 institutions in 2 countries.

Lin HanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Vikas MadanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore. csivm@nus.edu.sg.ORCID http://orcid.org/0000-0001-7876-624X
Anand MayakondaCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Pushkar DakleCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Teoh Weoi WoonCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Pavithra ShyamsunderCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Hazimah Binte Mohd NordinCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Zeya CaoCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Janani SundaresanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Ienglam LeiDepartment of Cardiac Surgery, Cardiovascular Research Center, University of Michigan, Ann Arbor, MI, USA.
Zhong WangDepartment of Cardiac Surgery, Cardiovascular Research Center, University of Michigan, Ann Arbor, MI, USA.
H Phillip KoefflerCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
National University of Singapore · SGUniversity of Michigan · USCedars-Sinai Medical Center · US

Funding

Epigenetic control of multipotent cardiac progenitor cell differentiationR01HL109054 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, ZHONG · 2012 to 2016
$1.9M
NHLBI NIH HHS R01 HL109054
6 · The paper itself

Abstract

Precise regulation of chromatin architecture is vital to physiological processes including hematopoiesis. ARID1A is a core component of the mammalian SWI/SNF complex, which is one of the ATP-dependent chromatin remodeling complexes. To uncover the role of ARID1A in hematopoietic development, we utilized hematopoietic cell-specific deletion of Arid1a in mice. We demonstrate that ARID1A is essential for maintaining the frequency and function of hematopoietic stem cells and its loss impairs the differentiation of both myeloid and lymphoid lineages. ARID1A deficiency led to a global reduction in open chromatin and ensuing transcriptional changes affected key genes involved in hematopoietic development. We also observed that silencing of ARID1A affected ATRA-induced differentiation of NB4 cells, suggesting its role in granulocytic differentiation of human leukemic cells. Overall, our study provides a comprehensive elucidation of the function of ARID1A in hematopoiesis and highlights the central role of ARID1A-containing SWI/SNF complex in maintaining chromatin dynamics in hematopoietic cells.

Indexed as

AnimalsCell DifferentiationCell LineageCell Line, TumorChromatinChromatin Assembly and DisassemblyDNA-Binding ProteinsHematopoiesisHumansMiceMice, Inbred C57BLMyeloid CellsTranscription FactorsArid1a protein, mouseChromatinDNA-Binding ProteinsTranscription Factors

Identifiers

PMID30858552
PMCPMC6756219
OpenAlexW2921552181

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.