Evidence map›Paper›PMID 41028752›Full record

ArticleNature communications2025

Cell-type-specific functionality encoded within the intrinsically disordered regions of OCT4.

Burak Ozkan, Mitzy Rios de Anda, Elisa Hall-Ponsele, Maria Rosa Portero Migueles, Amani Alshaikh, Marta Hanzevacki, Moriyah Naama, Katharine Furlong, Gareth A Roberts, Meryam Beniazza and 10 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

20 authors.

Burak Ozkan *Institute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0001-8850-2248
Mitzy Rios de Anda *Institute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Elisa Hall-PonseleInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Maria Rosa Portero MiguelesInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Amani AlshaikhInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Marta HanzevackiInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Moriyah NaamaDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Katharine FurlongInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Gareth A RobertsInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-3726-390X
Meryam BeniazzaInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
My Linh HuynhInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Michael R O'DwyerInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Sonia YiakoumiInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Christos SpanosWellcome Discovery Research Platform for Hidden Cell Biology, Michael Swann Building, Edinburgh, UK.ORCID http://orcid.org/0000-0002-4376-8242
Hazar YassenDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Keisuke KajiInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0001-5946-8415
Hitoshi NiwaInstitute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Yosef BuganimDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.ORCID http://orcid.org/0000-0002-7970-5163
Sally LowellInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-4018-9480
Abdenour SoufiInstitute of Regeneration and Repair, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK. Abdenour.Soufi@ed.ac.uk.ORCID http://orcid.org/0000-0002-3666-3266

Funding

Wellcome Trust 220298
6 · The paper itself

Abstract

The cell-type-specific function of transcription factors (TFs) is crucial for determining cellular identity. However, it is unclear how a single TF can function specifically in different cell types. Here, we define the molecular features that enable OCT4 to reprogram somatic cells into pluripotent or trophoblast stem cells, maintain the self-renewal of embryonic stem cells (ESCs), and drive lineage commitment during early embryonic development. Embedded within the intrinsically disordered regions (IDRs) of OCT4, we uncover short linear peptides that are essential for reprogramming (SLiPERs) but dispensable for ESC self-renewal. SLiPERs adopt a quasi-ordered state and, during reprogramming, recruit a unique set of proteins to closed chromatin that are unnecessary for ESC self-renewal. Interestingly, SLiPERs are essential for embryos to develop beyond late gastrulation. Removing SLiPERs leads to aberrant OCT4 binding, derailing the regular transition of ESCs out of pluripotency. Our findings identify modules within IDRs that contribute to the functional versatility and specificity of TFs.

Indexed as

Intrinsically Disordered ProteinsOctamer Transcription Factor-3AnimalsCellular ReprogrammingChromatinEmbryonic DevelopmentEmbryonic Stem CellsHumansMicePluripotent Stem CellsTrophoblastsChromatinIntrinsically Disordered ProteinsOctamer Transcription Factor-3Pou5f1 protein, mouse

Identifiers

PMID41028752
PMCPMC12485055

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.