Evidence map›Paper›PMID 38421638›Full record

ArticleNucleic acids research2024

HBO1 determines SMAD action in pluripotency and mesendoderm specification.

Cong Zhang, Yongli Shan, Huaisong Lin, Yanqi Zhang, Qi Xing, Jinmin Zhu, Tiancheng Zhou, Aiping Lin, Qianyu Chen, Junwei Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. 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

11 authors at 1 institution in 2 countries.

Cong ZhangKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Yongli ShanKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Huaisong LinKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Yanqi ZhangKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Qi XingKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Jinmin ZhuKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Tiancheng ZhouKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Aiping LinKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Qianyu ChenKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Junwei WangKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.
Guangjin PanKey Laboratory of Immune Response and Immunotherapy, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530,China; Guangzhou Medical University, Guangzhou 511436, China.ORCID 0000-0002-2378-7198
Guangzhou Institutes of Biomedicine and Health · CN

Funding

China Postdoctoral Science Foundation 2023M733516Guangdong Province Special Program for Outstanding Talents 2019JC05Y463Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine 2020B1212060052Guangzhou Key Research and Development Program 202206010041Health@InnoHK ProgramInnovation Technology Commission of the Hong Kong SAR, P. R. ChinaNational Key Research and Development Program of China 2022YFA1105001National Natural Science Foundation of China 32270624Science and Technology Planning Project of Guangdong Province 2023B1212060050University of Chinese Academy of Sciences Education Foundation ZXXM202201Youth Innovation Promotion Association of the Chinese Academy of Sciences 2022360
6 · The paper itself

Abstract

TGF-β signaling family plays an essential role to regulate fate decisions in pluripotency and lineage specification. How the action of TGF-β family signaling is intrinsically executed remains not fully elucidated. Here, we show that HBO1, a MYST histone acetyltransferase (HAT) is an essential cell intrinsic determinant for TGF-β signaling in human embryonic stem cells (hESCs). HBO1-/- hESCs fail to response to TGF-β signaling to maintain pluripotency and spontaneously differentiate into neuroectoderm. Moreover, HBO1 deficient hESCs show complete defect in mesendoderm specification in BMP4-triggered gastruloids or teratomas. Molecularly, HBO1 interacts with SMAD4 and co-binds the open chromatin labeled by H3K14ac and H3K4me3 in undifferentiated hESCs. Upon differentiation, HBO1/SMAD4 co-bind and maintain the mesoderm genes in BMP4-triggered mesoderm cells while lose chromatin occupancy in neural cells induced by dual-SMAD inhibition. Our data reveal an essential role of HBO1, a chromatin factor to determine the action of SMAD in both human pluripotency and mesendoderm specification.

Indexed as

Cell DifferentiationHistone AcetyltransferasesMesodermSignal TransductionSmad4 ProteinBone Morphogenetic Protein 4Cell LineChromatinEndodermHistonesHuman Embryonic Stem CellsHumansPluripotent Stem CellsTransforming Growth Factor betaBone Morphogenetic Protein 4ChromatinHistone AcetyltransferasesHistonesKAT7 protein, humanSmad4 ProteinSMAD4 protein, humanTransforming Growth Factor beta

Identifiers

PMID38421638
PMCPMC11109972
OpenAlexW4392297166

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.