ArticleNature communications2019
Maintenance of epigenetic landscape requires CIZ1 and is corrupted in differentiated fibroblasts in long-term culture.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 22 citations in OpenAlex.
- CIZ1 regulates G1 length and the CDK threshold for initiation of DNA replication to prevent DNA replication stress.Nucleic acids research · 2026Article
- Establishment and Maintenance of Repressed Chromatin States on Dosage-Compensated Sex Chromosomes.Biomolecules · 2026Review
- AURKB-driven dissolution of CIZ1-RNA assemblies from the inactive X chromosome in mitosis.Nucleic acids research · 2026Article
- Epigenetic deprogramming by disruption of CIZ1-RNA nuclear assemblies in early-stage breast cancers.The Journal of cell biology · 2025Article
- Epigenetic instability caused by absence of CIZ1 drives transformation during quiescence cycles.BMC biology · 2023Article
- CIZ1 in Xist seeded assemblies at the inactive X chromosome.Frontiers in cell and developmental biology · 2023Review
- Prion-like domains drive CIZ1 assembly formation at the inactive X chromosome.The Journal of cell biology · 2022Article
- Trans- and cis-acting effects of Firre on epigenetic features of the inactive X chromosome.Nature communications · 2020Article
- Akt1 and dCIZ1 promote cell survival from apoptotic caspase activation during regeneration and oncogenic overgrowth.Nature communications · 2020Article
- Identification of DHX9 as a cell cycle regulated nucleolar recruitment factor for CIZ1.Scientific reports · 2020Article
- Nonlinear sequence similarity between theRNA (New York, N.Y.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The inactive X chromosome (Xi) serves as a model for establishment and maintenance of repressed chromatin and the function of polycomb repressive complexes (PRC1/2). Here we show that Xi transiently relocates from the nuclear periphery towards the interior during its replication, in a process dependent on CIZ1. Compromised relocation of Xi in CIZ1-null primary mouse embryonic fibroblasts is accompanied by loss of PRC-mediated H2AK119Ub1 and H3K27me3, increased solubility of PRC2 catalytic subunit EZH2, and genome-wide deregulation of polycomb-regulated genes. Xi position in S phase is also corrupted in cells adapted to long-term culture (WT or CIZ1-null), and also accompanied by specific changes in EZH2 and its targets. The data are consistent with the idea that chromatin relocation during S phase contributes to maintenance of epigenetic landscape in primary cells, and that elevated soluble EZH2 is part of an error-prone mechanism by which modifying enzyme meets template when chromatin relocation is compromised.
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.