ArticleCell reports2017
Visualizing Changes in Cdkn1c Expression Links Early-Life Adversity to Imprint Mis-regulation in Adults.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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.
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.
Who cites it
34 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- Cell-cell communication-mediated cell-type-specific parent-of-origin effects in mammals.Nature communications · 2025Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- Perinatal nutrition as a key regulator of genomic imprinting: a new paradigm for maternal-child health.Frontiers in nutrition · 2025Article
- Epigenetic Mechanisms in Osteoporosis: Exploring the Power of mJournal of cellular and molecular medicine · 2025Review
- Differential CpG methylation at Nnat in the early establishment of beta cell heterogeneity.Diabetologia · 2024Article
- Protein restriction during pregnancy alters Cdkn1c silencing, dopamine circuitry and offspring behaviour without changing expression of key neuronal marker genes.Scientific reports · 2024Article
- Bioluminescence imaging of Cyp1a1-luciferase reporter mice demonstrates prolonged activation of the aryl hydrocarbon receptor in the lung.Communications biology · 2024Article
- Deficiency of the paternally-expressed imprintedFrontiers in neuroscience · 2024Article
- Epigenetic control of the imprinted growth regulatorEpigenetics · 2023Article
- Differential CpG methylation atbioRxiv : the preprint server for biology · 2023Article
- Imprinted genes and the manipulation of parenting in mammals.Nature reviews. Genetics · 2023Review
- Phenome-wide analyses identify an association between the parent-of-origin effects dependent methylome and the rate of aging in humans.Genome biology · 2023Article
- Drug-induced loss of imprinting revealed using bioluminescent reporters of Cdkn1c.Scientific reports · 2023Article
- Endogenous bioluminescent reporters reveal a sustained increase in utrophin gene expression upon EZH2 and ERK1/2 inhibition.Communications biology · 2023Article
- Epigenetic changes induced by in utero dietary challenge result in phenotypic variability in successive generations of mice.Nature communications · 2022Article
- In support of the placental programming hypothesis: Placental endocrine insufficiency programs atypical behaviour in mothers and their offspring.Experimental physiology · 2022Review
- Methylation status of nc886 epiallele reflects periconceptional conditions and is associated with glucose metabolism through nc886 RNAs.Clinical epigenetics · 2021Article
- Transcriptional analysis of sodium valproate in a serotonergic cell line reveals gene regulation through both HDAC inhibition-dependent and independent mechanisms.The pharmacogenomics journal · 2021Article
- Importance of Both Imprinted Genes and Functional Heterogeneity in Pancreatic Beta Cells: Is There a Link?International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
Imprinted genes are regulated according to parental origin and can influence embryonic growth and metabolism and confer disease susceptibility. Here, we designed sensitive allele-specific reporters to non-invasively monitor imprinted Cdkn1c expression in mice and showed that expression was modulated by environmental factors encountered in utero. Acute exposure to chromatin-modifying drugs resulted in de-repression of paternally inherited (silent) Cdkn1c alleles in embryos that was temporary and resolved after birth. In contrast, deprivation of maternal dietary protein in utero provoked permanent de-repression of imprinted Cdkn1c expression that was sustained into adulthood and occurred through a folate-dependent mechanism of DNA methylation loss. Given the function of imprinted genes in regulating behavior and metabolic processes in adults, these results establish imprinting deregulation as a credible mechanism linking early-life adversity to later-life outcomes. Furthermore, Cdkn1c-luciferase mice offer non-invasive tools to identify factors that disrupt epigenetic processes and strategies to limit their long-term impact.
Indexed as
Identifiers
What OpenQuestion holds
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.