Snail Mediates E-Cadherin Repression by the Recruitment of the Sin3A/Histone Deacetylase 1 (HDAC1)/HDAC2 Complex

By H. Peinado, Esteban Ballestar, Manel Esteller, A. Cano. Molecular and Cellular Biology, 2004

771 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a2d7793f609b30d7dd944fc3867af7473c90f8d7

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Citations in the corpus

The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “Snail-mediated cadherin repression and EMT is assisted by the recruitment of SIN3A, histone deacetylases, and components of the Polycomb 2 complex (Herranz et al. 2008, Peinado et al. 2004a).”
Repression of E-cadherin by the polycomb group protein EZH2 in cancer (2008, background): “…repression by snail and slug, ubiquitination and degradation of the E-cadherin and lysosomal targeting of the E-cadherin for degradation (Batlle et al., 2000; Fujita et al., 2002; Hajra et al., 2002; Peinado et al., 2004; Saito et al., 2004; Takeno et al., 2004; Palacios et al., 2005).”
New signals from the invasive front (2006, background): “The E-cadherin promoter is frequently repressed by specific transcriptional repressors, including Snail, Slug, SIP1, δEF1, Twist and E12/E47, and by subsequent promoter hypermethylatio”
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications (2016, background): “On the other hand, histone deacetylases (HDACs) catalyze the removal of the acetyl residues in the chromatin of inactive regions [31, 74, 75].”
Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling. (2010, background): “This is mediated by the amino-terminal SNAG domain of Snail, which recruits a histone deacetylase (Batlle et al. 2000; Peinado et al. 2004a).”
Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition (2010, background): “Snail interacts with HDAC1–HDAC2, AJUBA–PRMT5 or PRC2, to repress E-cadherin expressio”
E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, background): “members of the zinc finger homeobox (ZFH) family of repressors, ZEB1 and ZEB2 [3–14].”
Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “SNAI1 induces repressive histone modifications at the CDH1 promoter through recruiting transcription repressors such as HDACs and SIN3A (Peinado et al., 2004).”
DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells (2005, background): “…al., 2000), as well as repression by specific transcription factors, including Snail (Batlle et al., 2000; Cano et al., 2000; Guaita et al., 2002; Peinado et al., 2004b), Slug (Hajra et al., 2002; Bolos et al., 2003), Smad-interacting protein 1 (SIP1, ZEB2) (Comijn et al., 2001) and the…”
The Role of Snail in EMT and Tumorigenesis (2013, background): “For instance, Snail interacts with the Sin3A-HDAC1/2 complex through the SNAG domain to deacetylate histone H3 and H4, leading to the repression of E-cadherin expression [14].”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “transcription by recruiting co-repressors [82,83] and known repressor complexes [84,85] but also by influencing the activity of other E-”
The role of histone deacetylases (HDACs) in human cancer (2007, background): “The transcription factor Snail recruits HDAC1, HDAC2, and the corepressor complex mSin3A to the E-cadherin promoter to repress its expression (Peinado et al., 2004).”