The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A
Open accessAbstract
Sp1-like proteins are defined by three highly homologous C(2)H(2) zinc finger motifs that bind GC-rich sequences found in the promoters of a large number of genes essential for mammalian cell homeostasis. Here we report that TIEG2, a transforming growth factor beta-inducible Sp1-like protein with antiproliferative functions, represses transcription through recruitment of the mSin3A-histone deacetylase complex. The interaction of TIEG2 with mSin3A is mediated by an alpha-helical repression motif (alpha-HRM) located within the repression domain (R1) of TIEG2. This alpha-HRM specifically associates with the second paired amphipathic helix (PAH2) domain of mSin3A. Mutations in the TIEG2 alpha-HRM domain that disrupt its helical structure abolish its ability to both bind mSin3A and repress transcription. Interestingly, the alpha-HRM is conserved in both the TIEG (TIEG1 and TIEG2) and BTEB (BTEB1, BTEB3, and BTEB4) subfamilies of Sp1-like proteins. The alpha-HRM from these proteins also mediates direct interaction with mSin3A and represses transcription. Surprisingly, we found that the alpha-HRM of the Sp1-like proteins characterized here exhibits structural and functional resemblance to the Sin3A-interacting domain previously described for the basic helix-loop-helix protein Mad1. Thus, our study defines a mechanism of transcriptional repression via the interactions of the alpha-HRM with the Sin3-histone deacetylase complex that is utilized by at least five Sp1-like transcriptional factors. More importantly, we demonstrate that a helical repression motif which mediates Sin3 interaction is not an exclusive structural and functional characteristic of the Mad1 subfamily but rather has a wider functional impact on transcriptional repression than previously demonstrated.
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
The biology of the mammalian Krüppel-like family of transcription factors
Dang, D. T., Pevsner, J., & Yang, V. W. (2000) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/s1357-2725(00)00059-5 · Cited by 458
Cited by
Mammalian Krüppel-Like Factors in Health and Diseases
McConnell, B. B., & Yang, V. W. (2010) · Physiological Reviews · doi:10.1152/physrev.00058.2009 · Cited by 1,018
Krüppel-like factors in cancer
Tetreault, M.-P., Yang, Y., & Katz, J. P. (2013) · Nature Reviews Cancer · doi:10.1038/nrc3582 · Cited by 398
Neve, B., Fernandez-Zapico, M. E., Ashkenazi-Katalan, V., Dina, C., Hamid, Y. H., Joly, E., Vaillant, E., Benmezroua, Y., Durand, E., Bakaher, N., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0409177102 · Cited by 293
Self-citationPresnell, J. S., Schnitzler, C. E., & Browne, W. E. (2015) · Genome Biology and Evolution · doi:10.1093/gbe/evv141 · Cited by 119
Sun, J., Wang, B., Liu, Y., Zhang, L., Ma, A., Yang, Z., Ji, Y., & Liu, Y. (2014) · Cancer Letters · doi:10.1016/j.canlet.2014.09.022 · Cited by 83
Metadata
- Authors
- Zhang, J.-S., Moncrieffe, M. C., Kaczynski, J., Ellenrieder, V., Prendergast, F. G., & Urrutia, R.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2001-08-01
- Volume
- 21
- Issue
- 15
- Pages
- 5041-5049
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2171195379
- Cited by
- 186
- References
- 1
- FWCI
- 2.93
- 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: A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A. https://app.cochat.ai/papers/10.1128/mcb.21.15.5041-5049.2001
- The paper
- Zhang, J.-S., Moncrieffe, M. C., Kaczynski, J., Ellenrieder, V., Prendergast, F. G., & Urrutia, R. (2001). A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.21.15.5041-5049.2001
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.
