ArticleNature communications2014
A prominent and conserved role for YY1 in Xist transcriptional activation.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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Who cites it
87 citing papers in PubMed, 148 citations in OpenAlex.
- From inactivation to intervention: X chromosome silencing in disease pathogenesis and emerging therapeutic strategies.Genes & diseases · 2026Review
- UniversalEPI: robust prediction of cell type-specific and differential chromatin interactions from DNA sequence and chromatin accessibility.Nucleic acids research · 2026Article
- FGF4 initiates X-chromosome inactivation via activating YY1 and prompting loss of pluripotency factors.The EMBO journal · 2026Article
- Remodeling ofScience advances · 2026Article
- YY1 in prostate cancer: multidimensional oncogenicmechanisms and emerging therapeutic vulnerabilities.Journal of molecular histology · 2026Review
- Xist in X chromosome inactivation: mechanisms and disease relevance.Cell communication and signaling : CCS · 2025Review
- Impact of somatic XIST deletions on ongoing XIST expression and inactive X silencing and heterochromatin.Human molecular genetics · 2025Article
- The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025Review
- Reporter CRISPR screens decipher cis-regulatory and trans-regulatory principles at the Xist locus.Nature structural & molecular biology · 2025Article
- Sex differences in the developing human cortex intersect with genetic risk of neurodevelopmental disorders.bioRxiv : the preprint server for biology · 2025Article
- Xist condensates: perspectives for therapeutic intervention.Genome biology · 2025Review
- SARS-CoV-2 encoded ORF3a interacts with YY1 to promote latent HCMV reactivation.PLoS pathogens · 2025Article
- X chromosome inactivation in mammals: general principles and species-specific considerations.EMBO reports · 2025Review
- Gene reactivation upon erosion of X chromosome inactivation in female hiPSCs is predictable yet variable and persists through differentiation.Stem cell reports · 2025Article
- Transcriptional stochasticity reveals multiple mechanisms of long non-coding RNA regulation at the Xist-Tsix locus.Nature communications · 2025Article
- Human XIST: Origin and Divergence of aNon-coding RNA · 2025Review
- Recruitment of chromatin remodelers by XIST B-repeat region is variably dependent on HNRNPK.Human molecular genetics · 2025Article
- YY1 is a transcriptional activator of the mouse LINE-1 Tf subfamily.Nucleic acids research · 2024Article
- Multifaceted role of CTCF in X-chromosome inactivation.Chromosoma · 2024Review
- Establishment and maintenance of random monoallelic expression.Development (Cambridge, England) · 2024Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Accumulation of the noncoding RNA Xist on one X chromosome in female cells is a hallmark of X-chromosome inactivation (XCI) in eutherians. Here we uncover an essential function for the ubiquitous autosomal transcription factor Yin-Yang 1 (YY1) in the transcriptional activation of Xist in both human and mouse. We show that loss of YY1 prevents Xist upregulation during the initiation and maintenance of X-inactivation, and that YY1 binds directly the Xist 5' region to trigger the activity of the Xist promoter. Binding of YY1 to the Xist 5' region before XCI competes with the Xist repressor REX1, whereas DNA methylation controls mono-allelic fixation of YY1 to Xist at the onset of XCI. YY1 is thus the first autosomal activating factor involved in a fundamental and conserved pathway of Xist regulation that ensures the asymmetric transcriptional upregulation of the master regulator of XCI.
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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.