The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Ring1b-mediated H2A Ubiquitination Associates with Inactive X Chromosomes and Is Involved in Initiation of X Inactivation
Open accessAbstract
Histone modifications are thought to serve as epigenetic markers that mediate dynamic changes in chromatin structure and regulation of gene expression. As a model system for understanding epigenetic silencing, X chromosome inactivation has been previously linked to a number of histone modifications including methylation and hypoacetylation. In this study, we provide evidence that supports H2A ubiquitination as a novel epigenetic marker for the inactive X chromosome (Xi) and links H2A ubiquitination to initiation of X inactivation. We found that the H2A-K119 ubiquitin E3 ligase Ring1b, a Polycomb group protein, is enriched on Xi in female trophoblast stem (TS) cells as well as differentiating embryonic stem (ES) cells. Consistent with Ring1b mediating H2A ubiquitination, ubiquitinated H2A (ubH2A) is also enriched on the Xi of both TS and ES cells. We demonstrate that the enrichment of Ring1b and ubH2A on Xi is transient during TS and ES cell differentiation, suggesting that the Ring1b and ubH2A are involved in the initiation of both imprinted and random X inactivation. Furthermore, we showed that the association of Ring1b and ubH2A with Xi is mitotically stable in non-differentiated TS cells.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Role of Histone H3 Lysine 27 Methylation in Polycomb-Group Silencing
Cao, R., Wang, L., Wang, H., Xia, L., Erdjument-Bromage, H., Tempst, P., Jones, R. S., & Zhang, Y. (2002) · Science · doi:10.1126/science.1076997 · Cited by 3,775
Self-citationHenry, K. W., Wyce, A., Lo, W.-S., Duggan, L. J., Emre, N. C. T., Kao, C.-F., Pillus, L., Shilatifard, A., Osley, M. A., & Berger, S. L. (2003) · Genes & Development · doi:10.1101/gad.1144003 · Cited by 714
Histone H3 lysine 9 methylation is an epigenetic imprint of facultative heterochromatin
Peters, A. H. F. M., Mermoud, J. E., O'Carroll, D., Pagani, M., Schweizer, D., Brockdorff, N., & Jenuwein, T. (2002) · Nature Genetics · doi:10.1038/ng789 · Cited by 502
Cited by
The diverse functions of histone lysine methylation
Martin, C., & Zhang, Y. (2005) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1761 · Cited by 2,057
Self-citationHistones: annotating chromatin
Campos, E. I., & Reinberg, D. (2009) · Annual Review of Genetics · doi:10.1146/annurev.genet.032608.103928 · Cited by 852
Histone Ubiquitination: Triggering Gene Activity
Weake, V. M., & Workman, J. L. (2008) · Molecular Cell · doi:10.1016/j.molcel.2008.02.014 · Cited by 684
Facultative Heterochromatin: Is There a Distinctive Molecular Signature?
Trojer, P., & Reinberg, D. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.09.011 · Cited by 608
Tavares, L., Dimitrova, E., Oxley, D., Webster, J., Poot, R., Demmers, J., Bezstarosti, K., Taylor, S., Ura, H., Koide, H., et al. (2012) · Cell · doi:10.1016/j.cell.2011.12.029 · Cited by 555
Metadata
- Authors
- Fang, J., Chen, T., Chadwick, B., Li, E., & Zhang, Y.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2004-12
- Volume
- 279
- Issue
- 51
- Pages
- 52812-52815
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1991287841
- Cited by
- 249
- References
- 3
- FWCI
- 6.78
- Type
- journal article
- Language
- en
- Open access
- hybrid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Ring1b-mediated H2A Ubiquitination Associates with Inactive X Chromosomes and Is Involved in Initiation of X Inactivation. https://app.cochat.ai/papers/10.1074/jbc.c400493200
- The paper
- Fang, J., Chen, T., Chadwick, B., Li, E., & Zhang, Y. (2004). Ring1b-mediated H2A Ubiquitination Associates with Inactive X Chromosomes and Is Involved in Initiation of X Inactivation. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.c400493200
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.