The DOI matches its Crossref record; 98 of the 98 references it cites were found in a registry or an index.
YAP1 Exerts Its Transcriptional Control via TEAD-Mediated Activation of Enhancers
Open accessAbstract
YAP1 is a major effector of the Hippo pathway and a well-established oncogene. Elevated YAP1 activity due to mutations in Hippo pathway components or YAP1 amplification is observed in several types of human cancers. Here we investigated its genomic binding landscape in YAP1-activated cancer cells, as well as in non-transformed cells. We demonstrate that TEAD transcription factors mediate YAP1 chromatin-binding genome-wide, further explaining their dominant role as primary mediators of YAP1-transcriptional activity. Moreover, we show that YAP1 largely exerts its transcriptional control via distal enhancers that are marked by H3K27 acetylation and that YAP1 is necessary for this chromatin mark at bound enhancers and the activity of the associated genes. This work establishes YAP1-mediated transcriptional regulation at distal enhancers and provides an expanded set of target genes resulting in a fundamental source to study YAP1 function in a normal and cancer setting.
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.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“ChIP-seq and deepsequencing studies in cancer and normal cells showed that several YAP-binding regions also show a consensus motif for AP-1 transcriptional factors suggesting that YAP/TEAD and AP-1 cooperatively regulate target genes representing a cross-talk between YAP and JNK signalling (74,75).”
From A Tumour-Specific Molecular Network Promotes Tumour Growth in Drosophila by Enforcing a JNK-YKI Feedforward Loop (2023) · cites this paper as [74]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Third, YAP/TEAD bind distal regulatory elements to regulate transcription of target genes (73-75).”
From A Tumour-Specific Molecular Network Promotes Tumour Growth in Drosophila by Enforcing a JNK-YKI Feedforward Loop (2023) · cites this paper as [74]
The cited source says what the claim attributes to it.
In the citing paper
“Consistently, published ChIP-seq datasets34,38,39 reveal a similar phenomenon in human cancer cell lines (Figure S7F).”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [38]
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
Gene Ontology: tool for the unification of biology
Ashburner, M., Ball, C. A., Blake, J. A., Botstein, D., Butler, H., Cherry, J. M., Davis, A. P., Dolinski, K., Dwight, S. S., Eppig, J. T., et al. (2000) · Nature Genetics · doi:10.1038/75556 · Cited by 43,206
Ultrafast and memory-efficient alignment of short DNA sequences to the human genome.
Langmead, B., Trapnell, C., Pop, M., & Salzberg, S. L. (2009) · Genome Biology · doi:10.1186/gb-2009-10-3-r25 · Cited by 21,849
Model-based Analysis of ChIP-Seq (MACS)
Zhang, Y., Liu, T., Meyer, C. A., Eeckhoute, J., Johnson, D. S., Bernstein, B. E., Nusbaum, C., Myers, R. M., Brown, M., Li, W., et al. (2008) · Genome Biology · doi:10.1186/gb-2008-9-9-r137 · Cited by 18,386
Cerami, E., Gao, J., Dogrusoz, U., Gross, B. E., Sumer, S. O., Aksoy, B. A., Jacobsen, A., Byrne, C. J., Heuer, M. L., Larsson, E., et al. (2012) · Cancer Discovery · doi:10.1158/2159-8290.cd-12-0095 · Cited by 17,455
Differential expression analysis for sequence count data
Anders, S., & Huber, W. (2010) · Genome Biology · doi:10.1186/gb-2010-11-10-r106 · Cited by 15,581
Trapnell, C., Williams, B. A., Pertea, G., Mortazavi, A., Kwan, G., van Baren, M. J., Salzberg, S. L., Wold, B. J., & Pachter, L. (2010) · Nature Biotechnology · doi:10.1038/nbt.1621 · Cited by 15,556
Integrative Analysis of Complex Cancer Genomics and Clinical Profiles Using the cBioPortal
Gao, J., Aksoy, B. A., Dogrusoz, U., Dresdner, G., Gross, B., Sumer, S. O., Sun, Y., Jacobsen, A., Sinha, R., Larsson, E., et al. (2013) · Science Signaling · doi:10.1126/scisignal.2004088 · Cited by 15,160
The Human Genome Browser at UCSC
Kent, W. J., Sugnet, C. W., Furey, T. S., Roskin, K. M., Pringle, T. H., Zahler, A. M., & Haussler, A. D. (2002) · Genome Research · doi:10.1101/gr.229102 · Cited by 10,400
Histone H3K27ac separates active from poised enhancers and predicts developmental state
Creyghton, M. P., Cheng, A. W., Welstead, G. G., Kooistra, T., Carey, B. W., Steine, E. J., Hanna, J., Lodato, M. A., Frampton, G. M., Sharp, P. A., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1016071107 · Cited by 4,302
Evolutionarily conserved elements in vertebrate, insect, worm, and yeast genomes
Siepel, A., Bejerano, G., Pedersen, J. S., Hinrichs, A. S., Hou, M., Rosenbloom, K., Clawson, H., Spieth, J., Hillier, L. W., Richards, S., et al. (2005) · Genome Research · doi:10.1101/gr.3715005 · Cited by 3,971 · cited 1×
“We calculated the conservation rate of regions using the PhastCons 46 way placental mammals [94].”
Method
Flagged first, then by citations
Cited by
Sorted by citations
Items 401–415 of 415
CD98hc, une histoire au long cours(t)
Ibrahim, A. Y. (2023) · theses.fr (ABES) · doi:10.70675/4f8263c2za7cdz4fb6za204z666831bd12b6
Gautier, M., Kramdi, A., Louis‐Brennetot, C., Pierre‐Eugène, C., Zaïdi, S., Lossec, C., Raynal, V., Baulande, S., Delattre, O., Thirant, C., et al. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117351
Wang, Y., Nai, Z., & Zhang, J. (2026) · World Journal of Surgical Oncology · doi:10.1186/s12957-026-04391-7
Polz, M., Kainz, M. P., Haider, N., Rienmüller, T. M., Lenk, K., Kargl, R., Terzano, M., Sommer, G., Holzapfel, G. A., & Fuchs, J. (2026) · Advanced Healthcare Materials · doi:10.1002/adhm.71400 · Cited by 1
Tumor progression is effectively suppressed by miR-195 through direct targeting of YAP1
Xiao-wei, W., Song, J., Tang, M.-M., He, Y.-Y., & Cai, Z. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2026.1858597
Torres, J. A., Schonweiler, E., Thimraj, T. A., Liu, H., Springer, A. D., Murray, J. W., Saqi, A., & Snoeck, H. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.07.27.741036
Lin, Z., Luo, S., Zheng, M. L., Lin, Z., Luo, L., Zhang, D., Lian, X., Wang, X., Wang, S., & Sun, J. (2026) · Histochemistry and Cell Biology · doi:10.1007/s00418-026-02524-3
Xiang, Y., Li, Y., Tian, C., Gu, R., He, F., Wen, H., Xie, L., & Zhou, P. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.05.742921
Therapeutic targeting of FRMD6 ameliorates BMSC senescence through modulating Hippo/YAP signaling
Tao, Z., Xu, X., Ma, X., Zhang, X., Zhang, W., Yang, B., Zhan, H., Zhou, X., Wang, Q., Zhang, Z., et al. (2026) · Genes & Diseases · doi:10.1016/j.gendis.2026.102451
O'Donnell, M., Guglya, A., Ghorbanpour, E., Tijet, N., Notley, C. R. P., Bucciol, E., Azad, T., van Rensburg, H. J. J., Yang, X., & Lillicrap, D. (2026) · Journal of Thrombosis and Haemostasis · doi:10.1016/j.jtha.2026.09.034
YAP/TAZ as a mechanochemical signal-resolution circuit
Sailis, A. B. (2026) · Progress in Biophysics and Molecular Biology · doi:10.1016/j.pbiomolbio.2026.101960
Hippo signaling drives mesenchymal cell fate and heterogeneity in liver cancer
Souza, N. A., Kowalczyk, W., Soheily, S., Canoot, G., Ostyn, T., Corral-Ibáñez, M., Sarfi, M., Hillen, H., Sansores-García, L., Huffel, L. V., et al. (2026) · JHEP Reports · doi:10.1016/j.jhepr.2026.102064
BindingDB (2019) · UC San Diego · doi:10.7270/q24170g4
Kasai, A., Ito, S., Ushioda, R., & Nagata, K. (2026) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2026.113703
Metadata
- Authors
- Stein, C., Bardet, A. F., Roma, G., Bergling, S., Clay, I., Ruchti, A., Agarinis, C., Schmelzle, T., Bouwmeester, T., Schübeler, D., & Bauer, A.
- Affiliations
- Novartis (Switzerland) (CH)
- Friedrich Miescher Institute (CH)
- University of Basel (CH)
- Corresponding author
- Schübeler, Dirk
- Bauer, Andreas
- ORCID
- Venue
- PLOS Genetics
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-08-21
- Volume
- 11
- Issue
- 8
- Pages
- e1005465
- ISSN
- 1553-7390 (ISSN-L)
- 1553-7404
- PMC
- PMC4546604
- OpenAlex
- W1539804860
- Cited by
- 414
- References
- 98
- Citations by year
- 2026: 26 · 2025: 26 · 2024: 53 · 2023: 52 · 2022: 42 · 2021: 52 · 2020: 42 · 2019: 38 · 2018: 33 · 2017: 29 · 2016: 17 · 2015: 2
- FWCI
- 14.36
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS Genetics (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- European Commission (282510, 257082)
- SystemsX.ch
- FP7 Health (HEALTH-2010-257082, 282510)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- YAP, TEAD transcription factors, Hippo signaling pathway, enhancer activation, distal enhancers, H3K27 acetylation, chromatin binding, transcriptional regulation, oncogenes, cancer
- MeSH terms
- YAP-Signaling Proteins, TEA Domain Transcription Factors, Acetylation, Base Sequence, Binding Sites, DNA-Binding Proteins, Enhancer Elements, Genetic, Histones, Humans, Nuclear Proteins, Phosphoproteins, Protein Binding, Protein Processing, Post-Translational, Transcription Factors, Transcriptional Activation, Consensus Sequence, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, Transcriptome
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
