ArticleDevelopmental cell2021
Two sides of the Dlk1-Dio3 story in imprinting.
Article in Developmental cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed.
- Reciprocal, methylation-dependent binding of Zfp57 and Gzf1 safeguards Dlk1-Dio3 imprinting during developmental reprogramming.Nature communications · 2026Article
- EpiTyping: analysis of epigenetic aberrations in parental imprinting and X-chromosome inactivation using RNA-seq.Nature protocols · 2023Review
- Balanced gene dosage control rather than parental origin underpins genomic imprinting.Nature communications · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of imprinting (LOI) at the Dlk1-Dio3 locus is linked to Kagami-Ogata and Temple syndromes, and to cancer, but molecular mechanisms that prevent LOI are under-studied. In this issue of Developmental Cell, Aronson et al. demarcate the bipartite regulation of the Dlk1-Dio3 imprinting control region (ICR) IG-DMR, which maintains locus imprinting.
Indexed as
Identifiers
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Registered trials
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.