Evidence map›Paper›PMID 23658224›Full record

ArticleNucleic acids research2013

Mechanisms of in vivo binding site selection of the hematopoietic master transcription factor PU.1.

Thu-Hang Pham, Julia Minderjahn, Christian Schmidl, Helen Hoffmeister, Sandra Schmidhofer, Wei Chen, Gernot Längst, Christopher Benner, Michael Rehli

Abstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

68 citing papers in PubMed.

  1. Review
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  8. Cellular imbalance in proximal and distal lung of CFTRMolecular medicine (Cambridge, Mass.) · 2025
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  11. Transcriptional network dynamics in early T cell development.The Journal of experimental medicine · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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8 more citing papers are in PubMed but not listed here.

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

9 authors.

Thu-Hang PhamDepartment of Internal Medicine III, University Hospital Regensburg, F.-J.-Strauss Allee 11, D-93042 Regensburg, Germany.
Julia Minderjahn
Christian Schmidl
Helen Hoffmeister
Sandra Schmidhofer
Wei Chen
Gernot Längst
Christopher Benner
Michael Rehli

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor PU.1 is crucial for the development of many hematopoietic lineages and its binding patterns significantly change during differentiation processes. However, the 'rules' for binding or not-binding of potential binding sites are only partially understood. To unveil basic characteristics of PU.1 binding site selection in different cell types, we studied the binding properties of PU.1 during human macrophage differentiation. Using in vivo and in vitro binding assays, as well as computational prediction, we show that PU.1 selects its binding sites primarily based on sequence affinity, which results in the frequent autonomous binding of high affinity sites in DNase I inaccessible regions (25-45% of all occupied sites). Increasing PU.1 concentrations and the availability of cooperative transcription factor interactions during lineage differentiation both decrease affinity thresholds for in vivo binding and fine-tune cell type-specific PU.1 binding, which seems to be largely independent of DNA methylation. Occupied sites were predominantly detected in active chromatin domains, which are characterized by higher densities of PU.1 recognition sites and neighboring motifs for cooperative transcription factors. Our study supports a model of PU.1 binding control that involves motif-binding affinity, PU.1 concentration, cooperativeness with neighboring transcription factor sites and chromatin domain accessibility, which likely applies to all PU.1 expressing cells.

Indexed as

Base SequenceBinding SitesChromatinConsensus SequenceDeoxyribonuclease IDNAHumansMacrophagesMonocytesNucleotide MotifsProtein BindingProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Stem CellsTrans-ActivatorsChromatinDeoxyribonuclease IDNAProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID23658224
PMCPMC3711439

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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.