Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 323

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

Jpx RNA Activates Xist by Evicting CTCF

Open access
Sun, Sha, Del Rosario, Brian C., Szanto, Attila, Ogawa, Yuya, Jeon, Yesu, Lee, Jeannie T.·2013·Cell

Abstract

Summary In mammals, dosage compensation between XX and XY individuals occurs through X chromosome inactivation (XCI). The noncoding Xist RNA is expressed and initiates XCI only when more than one X chromosome is present. Current models invoke a dependency on the X-to-autosome ratio (X:A), but molecular factors remain poorly defined. Here, we demonstrate that molecular titration between an X-encoded RNA and an autosomally encoded protein dictates Xist induction. In pre-XCI cells, CTCF protein represses Xist transcription. At the onset of XCI, Jpx RNA is upregulated, binds CTCF, and extricates CTCF from one Xist allele. We demonstrate that CTCF is an RNA-binding protein and is titrated away from the Xist promoter by Jpx RNA. Thus, Jpx activates Xist by evicting CTCF. The functional antagonism via molecular titration reveals a role for long noncoding RNA in epigenetic regulation.

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.cell.2013.05.028

Cites

54 of 54 references verified0 citation errors · 0 not checkable

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.

A few free checks a day · papers already verified open instantly · results are public

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

1 retracted

Show all 54 references

Cited by

See all 323

Metadata

Authors
Sun, S., Del Rosario, B. C., Szanto, A., Ogawa, Y., Jeon, Y., & Lee, J. T.
Venue
Cell
Publisher
Elsevier BV
Published
2013-06
Volume
153
Issue
7
Pages
1537-1551
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2149710757
Cited by
323
References
54
FWCI
22.25
Type
journal article
Language
en
Open access
bronze

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: Jpx RNA Activates Xist by Evicting CTCF. https://app.cochat.ai/papers/10.1016/j.cell.2013.05.028
The paper
Sun, S., Del Rosario, B. C., Szanto, A., Ogawa, Y., Jeon, Y., & Lee, J. T. (2013). Jpx RNA Activates Xist by Evicting CTCF. Cell. https://doi.org/10.1016/j.cell.2013.05.028

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.