Evidence map›Paper›PMID 38302581›Full record

ReviewMolecular systems biology2024

Canalizing cell fate by transcriptional repression.

Bryce Lim, Katrin Domsch, Moritz Mall, Ingrid Lohmann

Open access · goldAbstract readReview
In one paragraph

Review in Molecular systems biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.3field-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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Epithelial Reprogramming and Transition during Pulmonary Bioengineering.bioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. 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

4 authors at 2 institutions in 2 countries.

Bryce Lim *Cell Fate Engineering and Disease Modeling Group, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, 69120, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-5688-3952
Katrin Domsch *Heidelberg University, Centre for Organismal Studies (COS) Heidelberg, Department of Developmental Biology and Cell Networks - Cluster of Excellence, Heidelberg, Germany.
Moritz MallCell Fate Engineering and Disease Modeling Group, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, 69120, Heidelberg, Germany. m.mall@dkfz.de.ORCID http://orcid.org/0000-0002-1278-2594
Ingrid LohmannHeidelberg University, Centre for Organismal Studies (COS) Heidelberg, Department of Developmental Biology and Cell Networks - Cluster of Excellence, Heidelberg, Germany. ingrid.lohmann@cos.uni-heidelberg.de.ORCID http://orcid.org/0000-0002-0918-2758
German Cancer Research Center · DEHeidelberg University · DE

Funding

Deutsche Forschungsgemeinschaft (DFG) 504019642Deutsche Forschungsgemeinschaft (DFG) 514206638Deutsche Forschungsgemeinschaft (DFG) LO 844/8-4EC | ERC | HORIZON EUROPE European Research Council (ERC) 804710
6 · The paper itself

Abstract

Precision in the establishment and maintenance of cellular identities is crucial for the development of multicellular organisms and requires tight regulation of gene expression. While extensive research has focused on understanding cell type-specific gene activation, the complex mechanisms underlying the transcriptional repression of alternative fates are not fully understood. Here, we provide an overview of the repressive mechanisms involved in cell fate regulation. We discuss the molecular machinery responsible for suppressing alternative fates and highlight the crucial role of sequence-specific transcription factors (TFs) in this process. Depletion of these TFs can result in unwanted gene expression and increased cellular plasticity. We suggest that these TFs recruit cell type-specific repressive complexes to their cis-regulatory elements, enabling them to modulate chromatin accessibility in a context-dependent manner. This modulation effectively suppresses master regulators of alternative fate programs and their downstream targets. The modularity and dynamic behavior of these repressive complexes enables a limited number of repressors to canalize and maintain major and minor cell fate decisions at different stages of development.

Indexed as

ChromatinTranscription FactorsCell DifferentiationGene ExpressionTranscriptional ActivationChromatinTranscription FactorsAlternative Fate RepressionCell Fate PlasticityCell IdentityEpigenetic SilencingTranscriptional Repressor

Identifiers

PMID38302581
PMCPMC10912439
OpenAlexW4391435778

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.