Evidence map›Paper›PMID 17785440›Full record

ArticleMolecular and cellular biology2007

The Pu.1 locus is differentially regulated at the level of chromatin structure and noncoding transcription by alternate mechanisms at distinct developmental stages of hematopoiesis.

Maarten Hoogenkamp, Hanna Krysinska, Richard Ingram, Gang Huang, Rachael Barlow, Deborah Clarke, Alexander Ebralidze, Pu Zhang, Hiromi Tagoh, Peter N Cockerill and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

37 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Runx1 promotes murine erythroid progenitor proliferation and inhibits differentiation by preventing Pu.1 downregulation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Review
  11. Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. The RUNX1-PU.1 axis in the control of hematopoiesis.International journal of hematology · 2015
    Review
  16. Article
  17. Article
  18. Review
  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.

Maarten HoogenkampUniversity of Leeds, Leeds Institute of Molecular Medicine, St. James's University Hospital, University of Leeds, Leeds LS9 7TF, United Kingdom.
Hanna Krysinska
Richard Ingram
Gang Huang
Rachael Barlow
Deborah Clarke
Alexander Ebralidze
Pu Zhang
Hiromi Tagoh
Peter N Cockerill
Daniel G Tenen
Constanze Bonifer
Harvard University · USSt James's University Hospital · GBUniversity of Leeds · GB

Funding

MOLECULAR BIOLOGY OF MYELOID DIFFERENTIATIONR01CA041456 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 1986 to 2010
$4.6M
Biotechnology and Biological Sciences Research Council G18655NCI NIH HHS CA41456NCI NIH HHS R01 CA041456Wellcome Trust
6 · The paper itself

Abstract

The Ets family transcription factor PU.1 is crucial for the regulation of hematopoietic development. Pu.1 is activated in hematopoietic stem cells and is expressed in mast cells, B cells, granulocytes, and macrophages but is switched off in T cells. Many of the transcription factors regulating Pu.1 have been identified, but little is known about how they organize Pu.1 chromatin in development. We analyzed the Pu.1 promoter and the upstream regulatory element (URE) using in vivo footprinting and chromatin immunoprecipitation assays. In B cells, Pu.1 was bound by a set of transcription factors different from that in myeloid cells and adopted alternative chromatin architectures. In T cells, Pu.1 chromatin at the URE was open and the same transcription factor binding sites were occupied as in B cells. The transcription factor RUNX1 was bound to the URE in precursor cells, but binding was down-regulated in maturing cells. In PU.1 knockout precursor cells, the Ets factor Fli-1 compensated for the lack of PU.1, and both proteins could occupy a subset of Pu.1 cis elements in PU.1-expressing cells. In addition, we identified novel URE-derived noncoding transcripts subject to tissue-specific regulation. Our results provide important insights into how overlapping, but different, sets of transcription factors program tissue-specific chromatin structures in the hematopoietic system.

Indexed as

Gene Expression Regulation, DevelopmentalTranscription, GeneticAnimalsBase SequenceB-LymphocytesCell DifferentiationCells, CulturedChromatinCore Binding Factor Alpha 2 SubunitHematopoiesisMacrophagesMiceMolecular Sequence DataMyeloid CellsNucleic Acid ConformationPromoter Regions, GeneticChromatinCore Binding Factor Alpha 2 SubunitProto-Oncogene ProteinsProto-Oncogene Protein Spi-1RNA, MessengerRNA Polymerase IIRNA, UntranslatedRunx1 protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID17785440
PMCPMC2169062
OpenAlexW1995040704

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.