The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
The connection between splicing and cancer
Open accessAbstract
Alternative splicing is a crucial mechanism for generating protein diversity. Different splice variants of a given protein can display different and even antagonistic biological functions. Therefore, appropriate control of their synthesis is required to assure the complex orchestration of cellular processes within multicellular organisms. Mutations in cis-acting splicing elements or changes in the activity of constitutive or alternative splicing could have a profound regulatory proteins that compromise the accuracy of either impact on human pathogenesis, in particular in tumor development and progression. Mutations in splicing elements, for example, have been found in genes such as LKB1, KIT, CDH17, KLF6 and BRCA1, and changes in trans-acting regulators can affect the expression of genes such as Ron, RAC1 and CD44.
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
New functions for the matrix metalloproteinases in cancer progression
Egeblad, M., & Werb, Z. (2002) · Nature Reviews Cancer · doi:10.1038/nrc745 · Cited by 6,108
Listening to silence and understanding nonsense: exonic mutations that affect splicing
Cartegni, L., Chew, S. L., & Krainer, A. R. (2002) · Nature Reviews Genetics · doi:10.1038/nrg775 · Cited by 2,209
Rac1b and reactive oxygen species mediate MMP-3-induced EMT and genomic instability
Radisky, D. C., Levy, D. D., Littlepage, L. E., Liu, H., Nelson, C. M., Fata, J. E., Leake, D., Godden, E. L., Albertson, D. G., Angela Nieto, M., et al. (2005) · Nature · doi:10.1038/nature03688 · Cited by 1,284
p53 isoforms can regulate p53 transcriptional activity
Bourdon, J.-C., Fernandes, K., Murray-Zmijewski, F., Liu, G., Diot, A., Xirodimas, D. P., Saville, M. K., & Lane, D. P. (2005) · Genes & Development · doi:10.1101/gad.1339905 · Cited by 810
The human SWI/SNF subunit Brm is a regulator of alternative splicing
Batsché, E., Yaniv, M., & Muchardt, C. (2006) · Nature Structural & Molecular Biology · doi:10.1038/nsmb1030 · Cited by 471
Signal-dependent regulation of splicing via phosphorylation of Sam68
Matter, N., Herrlich, P., & König, H. (2002) · Nature · doi:10.1038/nature01153 · Cited by 458
Giglio, S., Mancini, F., Gentiletti, F., Sparaco, G., Felicioni, L., Barassi, F., Martella, C., Prodosmo, A., Iacovelli, S., Buttitta, F., et al. (2005) · Cancer Research · doi:10.1158/0008-5472.can-05-0450 · Cited by 58
Cited by
Splicing in disease: disruption of the splicing code and the decoding machinery
Wang, G.-S., & Cooper, T. A. (2007) · Nature Reviews Genetics · doi:10.1038/nrg2164 · Cited by 1,050
Alternative splicing: a pivotal step between eukaryotic transcription and translation
Kornblihtt, A. R., Schor, I. E., Alló, M., Dujardin, G., Petrillo, E., & Muñoz, M. J. (2013) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3525 · Cited by 853
Self-citationBrown, R. L., Reinke, L. M., Damerow, M. S., Perez, D., Chodosh, L. A., Yang, J., & Cheng, C. (2011) · Journal of Clinical Investigation · doi:10.1172/jci44540 · Cited by 631
Anczuków, O., Rosenberg, A. Z., Akerman, M., Das, S., Zhan, L., Karni, R., Muthuswamy, S. K., & Krainer, A. R. (2012) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2207 · Cited by 447
Ward, A. J., & Cooper, T. A. (2010) · The Journal of Pathology · doi:10.1002/path.2649 · Cited by 414
Metadata
- Authors
- Srebrow, A., & Kornblihtt, A. R.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2006-07-01
- Volume
- 119
- Issue
- 13
- Pages
- 2635-2641
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2165090547
- Cited by
- 335
- References
- 7
- FWCI
- 9.70
- Type
- journal article
- Language
- en
- Open access
- green
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: The connection between splicing and cancer. https://app.cochat.ai/papers/10.1242/jcs.03053
- The paper
- Srebrow, A., & Kornblihtt, A. R. (2006). The connection between splicing and cancer. Journal of Cell Science. https://doi.org/10.1242/jcs.03053
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.
