Evidence map›Paper›PMID 31775036›Full record

ArticleCell reports2019

MLL1 Inhibition and Vitamin D Signaling Cooperate to Facilitate the Expanded Pluripotency State.

Hui Zhang, Le Tran Phuc Khoa, Fengbiao Mao, Hanshi Xu, Bo Zhou, Yu Han, Monique O'Leary, Asma Nusrat, Li Wang, Thomas L Saunders and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
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  6. Epigenetic regulation of mouse preimplantation embryo development.Current opinion in genetics & development · 2020
    Review
  7. 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 2 institutions in 2 countries.

Hui ZhangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; Department of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Le Tran Phuc KhoaDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Fengbiao MaoDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Hanshi XuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
Bo ZhouDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Yu HanState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
Monique O'LearyDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Asma NusratDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Li WangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
Thomas L SaundersDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Yali DouDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: yalid@med.umich.edu.
University of Michigan–Ann Arbor · USChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

Intestinal Mucosal Wound Resealing in IBDR01DK055679 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2004 to 2026
$8.1M
Function of MLL in transcription regulationR01GM082856 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DOU, YALI · 2009 to 2023
$4.0M
INTESTINAL MUCOSAL WOUND RESEALING IN SURGICAL DISEASESR29DK055679 · NIDDK · EMORY UNIVERSITY · PI NUSRAT, ASMA · 1998 to 2002
$324k
NIDDK NIH HHS R01 DK055679NIDDK NIH HHS R29 DK055679NIGMS NIH HHS R01 GM082856
6 · The paper itself

Abstract

Dynamic establishment of histone modifications in early development coincides with programed cell fate restriction and loss of totipotency beyond the early blastocyst stage. Causal function of histone-modifying enzymes in this process remains to be defined. Here we show that inhibiting histone methyltransferase MLL1 reprograms naive embryonic stem cells (ESCs) to expanded pluripotent stem cells (EPSCs), with differentiation potential toward both embryonic and extraembryonic lineages in vitro and in vivo. MLL1 inhibition or deletion upregulates gene signatures of early blastomere development. The function of MLL1 in restricting induction of EPSCs is mediated partly by Gc, which regulates cellular response to vitamin D signaling. Combined treatment of MLL1 inhibitor and 1α,25-dihydroxyvitamin D

Indexed as

Cell DifferentiationHistone-Lysine N-MethyltransferaseHumansMyeloid-Lymphoid Leukemia ProteinPluripotent Stem CellsSignal TransductionVitamin DHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinVitamin D2Cexpanded pluripotencyGchistone methylationMLL1preimplantation blastomeretotipotencyTSC-like cellsvitamin DWDR5 inhibitor

Identifiers

PMID31775036
PMCPMC9119704
OpenAlexW2990740093

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.