Evidence map›Paper›PMID 33058869›Full record

ArticleJournal of molecular biology2020

TET1 Interacts Directly with NANOG via Independent Domains Containing Hydrophobic and Aromatic Residues.

Raphaël Pantier, Nicholas Mullin, Elisa Hall-Ponsele, Ian Chambers

Open access · hybridAbstract read
In one paragraph

Article in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
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 1 institution in 1 country.

Raphaël PantierCentre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, 5 Little France Drive, Edinburgh EH16 4UU, Scotland, United Kingdom.
Nicholas MullinCentre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, 5 Little France Drive, Edinburgh EH16 4UU, Scotland, United Kingdom.
Elisa Hall-PonseleCentre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, 5 Little France Drive, Edinburgh EH16 4UU, Scotland, United Kingdom.
Ian ChambersCentre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, 5 Little France Drive, Edinburgh EH16 4UU, Scotland, United Kingdom. Electronic address: ichambers@ed.ac.uk.
University of Edinburgh · GB

Funding

Medical Research Council MR/K017047/1Medical Research Council MR/L018497/1Medical Research Council MR/T003162/1
6 · The paper itself

Abstract

The DNA demethylase TET1 is highly expressed in embryonic stem cells and is important both for lineage commitment, and reprogramming to naïve pluripotency. TET1 interacts with the pluripotency transcription factor NANOG which may contribute to its biological activity in pluripotent cells. However, how TET1 interacts with other proteins is largely unknown. Here, we characterise the physical interaction between TET1 and NANOG using embryonic stem cells and bacterial expression systems. TET1 and NANOG interact through multiple binding sites that act independently. Critically, mutating conserved hydrophobic and aromatic residues within TET1 and NANOG abolishes the interaction. On chromatin, NANOG is predominantly localised at ESC enhancers. While TET1 binds to CpG dinucleotides in promoters using its CXXC domain, TET1 also binds to enhancers, though the mechanism involved is unknown. Comparative ChIP-seq analysis identifies genomic loci bound by both TET1 and NANOG, that correspond predominantly to pluripotency enhancers. Importantly, around half of NANOG transcriptional target genes are associated with TET1-NANOG co-bound sites. These results indicate a mechanism by which TET1 protein may be targeted to specific sites of action at enhancers by direct interaction with a transcription factor.

Indexed as

AnimalsCellular ReprogrammingChromatinDNA-Binding ProteinsEmbryonic Stem CellsEnhancer Elements, GeneticHydrophobic and Hydrophilic InteractionsMiceNanog Homeobox ProteinProtein DomainsProto-Oncogene ProteinsTranscription FactorsChromatinDNA-Binding ProteinsNanog Homeobox ProteinProto-Oncogene ProteinsTET1 protein, mouseTranscription Factorschromatinembryonic stem cellsenhancerspluripotencyprotein–protein interactions

Identifiers

PMID33058869
PMCPMC7763487
OpenAlexW3093071547

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.