Evidence map›Paper›PMID 31712708›Full record

ArticleScientific reports2019

FOXH1 Is Regulated by NANOG and LIN28 for Early-stage Reprogramming.

Ling Wang, Yue Su, Chang Huang, Yexuan Yin, Jiaqi Zhu, Alec Knupp, Alexander Chu, Young Tang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Ling WangDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Yue SuDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Chang HuangDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Yexuan YinDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Jiaqi ZhuDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Alec KnuppDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Alexander ChuDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA.
Young TangDepartment of Animal Science, Institute for Systems Genomics, University of Connecticut, 1390 Storrs Rd, Storrs, CT, 06269, USA. yong.tang@uconn.edu.ORCID http://orcid.org/0000-0001-6188-7758
University of Connecticut · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FOXH1 is a primitive-streak specifier and ACTIVIN co-effector that plays an important role in development, and positively regulates the generation of human induced pluripotent stem cells (iPSCs) from somatic cells by OCT4, SOX2, KLF4, and MYC (OSKM) transduction. However, the mechanism and upstream regulation for FOXH1 expression in reprogramming are unclear. We found FOXH1 expression plays a significant role to enhance epithelial marker and suppress mesenchymal gene expression in OSKM-mediated human cell reprogramming. Furthermore, NANOG and LIN28 (NL) co-stimulate FOXH1 expression, which correlates with the enhanced reprogramming efficiency by NL-factors. FOXH1 expression is also stimulated by a specific inhibitor for H3K79 methyltransferase DOT1L (iDOT1L) but not by inhibition of the canonical WNT signaling. We further show that blocking endogenous FOXH1 expression eliminates the enhanced reprogramming effect by NL and iDOT1L. However, overexpressing FOXH1 in NL plus iDOT1L condition results in significantly reduced TRA-1-60 positively expressed cells and decreases pluripotent marker expression in reprogramming. Our study elucidated an essential role for properly stimulated FOXH1 expression by NANOG, LIN28, and H3K79 demethylation for dramatic enhancement of reprograming.

Indexed as

Gene Expression RegulationCellular ReprogrammingForkhead Transcription FactorsGene Knockdown TechniquesHumansKruppel-Like Factor 4Nanog Homeobox ProteinProto-Oncogene Proteins c-metRNA-Binding ProteinsWnt ProteinsForkhead Transcription FactorsFOXH1 protein, humanKLF4 protein, humanKruppel-Like Factor 4Lin28A protein, humanMET protein, humanNanog Homeobox ProteinNANOG protein, humanProto-Oncogene Proteins c-metRNA-Binding ProteinsWnt Proteins

Identifiers

PMID31712708
PMCPMC6848184
OpenAlexW2984727121

What OpenQuestion holds

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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.