Evidence map›Paper›PMID 38701780›Full record

ArticleStem cell reports2024

H1FOO-DD promotes efficiency and uniformity in reprogramming to naive pluripotency.

Akira Kunitomi, Ryoko Hirohata, Mitsujiro Osawa, Kaho Washizu, Vanessa Arreola, Norikazu Saiki, Tomoaki M Kato, Masaki Nomura, Haruko Kunitomi, Tokiko Ohkame and 11 more

Abstract read
In one paragraph

Article in Stem cell reports, 2024. 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. Article
  2. Review
  3. 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

21 authors.

Akira KunitomiCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA. Electronic address: akira.kunitomi@gladstone.ucsf.edu.
Ryoko HirohataCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; CiRA Foundation, Kyoto 606-8397, Japan.
Mitsujiro OsawaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Kaho WashizuGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
Vanessa ArreolaGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
Norikazu SaikiCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Tomoaki M KatoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; CiRA Foundation, Kyoto 606-8397, Japan.
Masaki NomuraCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; CiRA Foundation, Kyoto 606-8397, Japan.
Haruko KunitomiGladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
Tokiko OhkameCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Yusuke OhkameCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Jitsutaro KawaguchiID Pharma Co., Ltd, Ibaraki 300-2611, Japan.
Hiroto HaraID Pharma Co., Ltd, Ibaraki 300-2611, Japan.
Kohji KusanoID Pharma Co., Ltd, Ibaraki 300-2611, Japan.
Takuya YamamotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; Institute for the Advanced Study of Human Biology (WPI-ASHBi), Kyoto University, Kyoto 606-8501, Japan; Medical-risk Avoidance Based on iPS Cells Team, RIKEN Center for Advanced Intelligence Project (AIP), Kyoto 606-8507, Japan.
Yasuhiro TakashimaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Shugo TohyamaDepartment of Cardiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Shinsuke YuasaDepartment of Cardiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Keiichi FukudaDepartment of Cardiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Naoko TakasuCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; CiRA Foundation, Kyoto 606-8397, Japan.
Shinya YamanakaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA; CiRA Foundation, Kyoto 606-8397, Japan; Department of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterogeneity among both primed and naive pluripotent stem cell lines remains a major unresolved problem. Here we show that expressing the maternal-specific linker histone H1FOO fused to a destabilizing domain (H1FOO-DD), together with OCT4, SOX2, KLF4, and LMYC, in human somatic cells improves the quality of reprogramming to both primed and naive pluripotency. H1FOO-DD expression was associated with altered chromatin accessibility around pluripotency genes and with suppression of the innate immune response. Notably, H1FOO-DD generates naive induced pluripotent stem cells with lower variation in transcriptome and methylome among clones and a more uniform and superior differentiation potency. Furthermore, we elucidated that upregulation of FKBP1A, driven by these five factors, plays a key role in H1FOO-DD-mediated reprogramming.

Indexed as

Cellular ReprogrammingHistonesInduced Pluripotent Stem CellsKruppel-Like Factor 4Cell DifferentiationChromatinHumansKruppel-Like Transcription FactorsPluripotent Stem CellsSOXB1 Transcription FactorsTranscription FactorsTranscriptomeChromatinHistonesKruppel-Like Factor 4Kruppel-Like Transcription FactorsSOXB1 Transcription FactorsTranscription Factorsdestabilized domainFKBP1AH1FOOheterogeneityinduced pluripotent stem cellinnate immune responsenaive pluripotencyprimed pluripotencyreprogrammingSendai virus vector

Identifiers

PMID38701780
PMCPMC11103934

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Registered trials

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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.