Evidence map›Paper›PMID 35297517›Full record

ArticleCell proliferation2022

Heterozygous loss of Zbtb38 leads to early embryonic lethality via the suppression of Nanog and Sox2 expression.

Miki Nishio, Takuya Matsuura, Shunya Hibi, Shiomi Ohta, Chio Oka, Noriaki Sasai, Yasumasa Ishida, Eishou Matsuda

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 12 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 2 institutions in 1 country.

Miki NishioFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.
Takuya MatsuuraFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.
Shunya HibiFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.
Shiomi OhtaFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.
Chio OkaFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.
Noriaki SasaiDevelopment Biomedical Science, Nara Institute of Science and Technology, Ikoma, Japan.
Yasumasa IshidaFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.
Eishou MatsudaFunctional Genomics and Medicine, Nara Institute of Science and Technology, Ikoma, Japan.ORCID https://orcid.org/0000-0002-8008-4552
Nara Institute of Science and Technology · JPCosmo Bio (Japan) · JP

Funding

Japan Society for the Promotion of Science 16K08587
6 · The paper itself

Abstract

objectivesMammalian DNA methyltransferases are essential to re-establish global DNA methylation patterns during implantation, which is critical for transmitting epigenetic information to the next generation. In contrast, the significance of methyl-CpG binding proteins (MBPs) that bind methylated CpG remains almost unknown at this stage. We previously demonstrated that Zbtb38 (also known as CIBZ)-a zinc finger type of MBP-is required for mouse embryonic stem (ES) cell proliferation by positively regulating Nanog expression. However, the physiological function of Zbtb38 in vivo remains unclear. MATERIALS AND

methodsThis study used the Cre-loxP system to generate conditional Zbtb38 knockout mice. Cell proliferation and apoptosis were studied by immunofluorescence staining. Quantitative real-time PCR, immunoblotting and immunofluorescence were performed to investigate the molecular mechanisms.

resultsGermline loss of the Zbtb38 single allele resulted in decreased epiblast cell proliferation and increased apoptosis shortly after implantation, leading to early embryonic lethality. Heterozygous loss of Zbtb38 reduced the expression of Nanog, Sox2, and the genes responsible for epiblast proliferation, differentiation, and cell viability. Although this early lethal phenotype, Zbtb38 is dispensable for ES cell establishment and identity.

conclusionsThese findings indicate that Zbtb38 is essential for early embryonic development via the suppression of Nanog and Sox2 expression.

Indexed as

Embryonic Stem CellsZinc FingersAnimalsCell DifferentiationDNA MethylationHomeodomain ProteinsMammalsMiceMouse Embryonic Stem CellsNanog Homeobox ProteinOctamer Transcription Factor-3Repressor ProteinsHomeodomain ProteinsNanog Homeobox ProteinOctamer Transcription Factor-3Repressor ProteinsZbtb38 protein, mouse

Identifiers

PMID35297517
PMCPMC9055898
OpenAlexW4221082193

What OpenQuestion holds

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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.