ArticleThe Journal of biological chemistry2009
MAD2B, a novel TCF4-binding protein, modulates TCF4-mediated epithelial-mesenchymal transdifferentiation.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 66 citations in OpenAlex.
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- Probing hot spots of protein-protein interactions mediated by the safety-belt region of REV7.Structure (London, England : 1993) · 2024Article
- AURKB promotes bladder cancer progression by deregulating the p53 DNA damage response pathway via MAD2L2.Journal of translational medicine · 2024Article
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- REV7 in Cancer Biology and Management.Cancers · 2023Review
- Review
- Mitotic Arrest-Deficient 2 Like 2 (MAD2L2) Interacts withLife (Basel, Switzerland) · 2021Article
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- Low-Dose Nicotine Activates EGFR Signaling via α5-nAChR and Promotes Lung Adenocarcinoma Progression.International journal of molecular sciences · 2020Article
- SHLD2/FAM35A co-operates with REV7 to coordinate DNA double-strand break repair pathway choice.The EMBO journal · 2018Article
- MAD2B acts as a negative regulatory partner of TCF4 on proliferation in human dermal papilla cells.Scientific reports · 2017Article
- Exploring the role of sphingolipid machinery during the epithelial to mesenchymal transition program using an integrative approach.Oncotarget · 2016Article
- MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1.The Journal of biological chemistry · 2016Article
- High expression of REV7 is an independent prognostic indicator in patients with diffuse large B-cell lymphoma treated with rituximab.International journal of hematology · 2015Article
- Glucocorticoid Receptor β Acts as a Co-activator of T-Cell Factor 4 and Enhances Glioma Cell Proliferation.Molecular neurobiology · 2015Article
- Protein tyrosine phosphatase PTPN3 inhibits lung cancer cell proliferation and migration by promoting EGFR endocytic degradation.Oncogene · 2015Article
- Destabilization of pluripotency in the absence of Mad2l2.Cell cycle (Georgetown, Tex.) · 2015Article
- Rev7/Mad2B plays a critical role in the assembly of a functional mitotic spindle.Cell cycle (Georgetown, Tex.) · 2015Article
- REV7 is essential for DNA damage tolerance via two REV3L binding sites in mammalian DNA polymerase ζ.Nucleic acids research · 2015Article
- A critical function of Mad2l2 in primordial germ cell development of mice.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell factor 4 (TCF4) interacts with beta-catenin in the WNT signaling pathway and transactivates downstream target genes involved in cancer progression. To identify proteins that regulate TCF4-mediated biological responses, we performed a yeast two-hybrid screen to search for a TCF4-binding protein(s) and found that MAD2B interacts with TCF4. We confirmed that MAD2B is a TCF4-binding protein by co-immunoprecipitation. Using the TOPFLASH reporter assay, we found that MAD2B blocks TCF4-mediated transactivation. The MAD2B binding regions of TCF4 were identified by TCF4 deletion mapping and electrophoretic mobility shift assay analysis. TCF4 and MAD2B interactions abolished the DNA binding ability of TCF4. Knockdown of MAD2B in SW480 colorectal cancer cells led to the conversion of epithelial cells to a mesenchymal fibroblastoid phenotype (epithelial-mesenchymal transdifferentiation). An E-cadherin promoter reporter analysis showed that MAD2B modulates TCF4-mediated E-cadherin expression. MAD2B knockdown blocked E-cadherin expression and significantly induced mesenchymal markers, such as N-cadherin and vimentin. Mesenchymal induction was accompanied by F-actin redistribution and the appearance of a fibroblastoid phenotype. MAD2B knockdown also increased both mRNA and protein levels of Slug, a known TCF4-induced E-cadherin transcriptional repressor. A chromatin immunoprecipitation assay showed that MAD2B silencing enhances the ability of TCF4 to bind the Slug promoter. Thus, MAD2B is a novel TCF4-interacting protein. This study provides the first evidence for the involvement of MAD2B in TCF4-mediated epithelial-mesenchymal transdifferentiation.
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