Evidence map›Paper›PMID 37414790›Full record

ArticleNature communications2023

TET2 and TET3 loss disrupts small intestine differentiation and homeostasis.

Ihab Ansari, Llorenç Solé-Boldo, Meshi Ridnik, Julian Gutekunst, Oliver Gilliam, Maria Korshko, Timur Liwinski, Birgit Jickeli, Noa Weinberg-Corem, Michal Shoshkes-Carmel and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  4. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

14 authors at 4 institutions in 3 countries.

Ihab Ansari *Department of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel.ORCID 0000-0002-5076-5795
Llorenç Solé-Boldo *Division of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, Heidelberg, Germany.
Meshi RidnikDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel.
Julian GutekunstDivision of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, Heidelberg, Germany.
Oliver GilliamDivision of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-6277-4293
Maria KorshkoDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel.
Timur LiwinskiDepartment of Immunology, The Weizmann Institute of Science, Rehovot, Israel.
Birgit JickeliDepartment of Immunology, The Weizmann Institute of Science, Rehovot, Israel.ORCID 0000-0002-9628-0152
Noa Weinberg-CoremDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel.
Michal Shoshkes-CarmelDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel.ORCID 0000-0002-8406-2158
Eli PikarskyThe Lautenberg Center for Immunology, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel.ORCID 0000-0003-4186-7105
Eran ElinavDepartment of Immunology, The Weizmann Institute of Science, Rehovot, Israel.ORCID 0000-0002-5775-2110
Frank LykoDivision of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-4873-5431
Yehudit BergmanDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University Medical School, Jerusalem, Israel. Yehudit.bergman@mail.huji.ac.il.ORCID 0000-0001-6936-234X
Hebrew University of Jerusalem · ILGerman Cancer Research Center · DEUniversity of Basel · CHWeizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TET2/3 play a well-known role in epigenetic regulation and mouse development. However, their function in cellular differentiation and tissue homeostasis remains poorly understood. Here we show that ablation of TET2/3 in intestinal epithelial cells results in a murine phenotype characterized by a severe homeostasis imbalance in the small intestine. Tet2/3-deleted mice show a pronounced loss of mature Paneth cells as well as fewer Tuft and more Enteroendocrine cells. Further results show major changes in DNA methylation at putative enhancers, which are associated with cell fate-determining transcription factors and functional effector genes. Notably, pharmacological inhibition of DNA methylation partially rescues the methylation and cellular defects. TET2/3 loss also alters the microbiome, predisposing the intestine to inflammation under homeostatic conditions and acute inflammation-induced death. Together, our results uncover previously unrecognized critical roles for DNA demethylation, possibly occurring subsequently to chromatin opening during intestinal development, culminating in the establishment of normal intestinal crypts.

Indexed as

DioxygenasesEpigenesis, GeneticAnimalsCell DifferentiationDNA-Binding ProteinsDNA MethylationHomeostasisInflammationIntestine, SmallMiceDioxygenasesDNA-Binding ProteinsTet2 protein, mouseTet3 protein, mouse

Identifiers

PMID37414790
PMCPMC10326054
OpenAlexW4383313692

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.