ArticlePloS one2012
Characterization of the SNAG and SLUG domains of Snail2 in the repression of E-cadherin and EMT induction: modulation by serine 4 phosphorylation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Mechanism of LPS-activated gingival fibroblasts promote the migration of gastric cancer cells via CXCL12/CXCR4-Snail2-EMT axis.In vitro cellular & developmental biology. Animal · 2026Article
- NAD(H)-dependent corepressor CTBP1 integrates metabolic signals to drive oncogenic programs.Frontiers in immunology · 2026Review
- Elevated SNHG1 promotes invasion and migration of Cd(II)-transformed cells through Sox2, Rac1, and Slug.Toxicology and applied pharmacology · 2025Article
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025Review
- Control of Snail1 protein stability by post-translational modifications: the basis for a complex regulation of Snail1 function.International journal of biological sciences · 2025Review
- Potential role of epithelial-mesenchymal transition induced by periodontal pathogens in oral cancer.Journal of cellular and molecular medicine · 2024Review
- Unpacking the Complexity of Epithelial Plasticity: From Master Regulator Transcription Factors to Non-Coding RNAs.Cancers · 2023Review
- A Novel Gemcitabine-Resistant Gallbladder Cancer Model Provides Insights into Molecular Changes Occurring during Acquired Resistance.International journal of molecular sciences · 2023Article
- Post-Translational Modification of ZEB Family Members in Cancer Progression.International journal of molecular sciences · 2022Review
- CBP-mediated Slug acetylation stabilizes Slug and promotes EMT and migration of breast cancer cells.Science China. Life sciences · 2021Article
- The Post-Translational Regulation of Epithelial-Mesenchymal Transition-Inducing Transcription Factors in Cancer Metastasis.International journal of molecular sciences · 2021Review
- The role of epithelial-mesenchymal transition-regulating transcription factors in anti-cancer drug resistance.Archives of pharmacal research · 2021Review
- Disruption of Cell-Cell Communication in Anaplastic Thyroid Cancer as an Immunotherapeutic Opportunity.Advances in experimental medicine and biology · 2021Article
- Molecular regulation of Snai2 in development and disease.Journal of cell science · 2019Review
- SNAI1 recruits HDAC1 to suppress SNAI2 transcription during epithelial to mesenchymal transition.Scientific reports · 2019Article
- Epithelial-mesenchymal plasticity-engaging stemness in an interplay of phenotypes.Stem cell investigation · 2019Review
- Roles of the Phosphorylation of Transcriptional Factors in Epithelial-Mesenchymal Transition.Journal of oncology · 2019Review
- Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma.Cancer management and research · 2019Review
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Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Snail1 and Snail2, two highly related members of the Snail superfamily, are direct transcriptional repressors of E-cadherin and EMT inducers. Previous comparative gene profiling analyses have revealed important differences in the gene expression pattern regulated by Snail1 and Snail2, indicating functional differences between both factors. The molecular mechanism of Snail1-mediated repression has been elucidated to some extent, but very little is presently known on the repression mediated by Snail2. In the present work, we report on the characterization of Snail2 repression of E-cadherin and its regulation by phosphorylation. Both the N-terminal SNAG and the central SLUG domains of Snail2 are required for efficient repression of the E-cadherin promoter. The co-repressor NCoR interacts with Snail2 through the SNAG domain, while CtBP1 is recruited through the SLUG domain. Interestingly, the SNAG domain is absolutely required for EMT induction while the SLUG domain plays a negative modulation of Snail2 mediated EMT. Additionally, we identify here novel in vivo phosphorylation sites at serine 4 and serine 88 of Snail2 and demonstrate the functional implication of serine 4 in the regulation of Snail2-mediated repressor activity of E-cadherin and in Snail2 induction of EMT.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.