The Mouse Snail Gene Encodes a Key Regulator of the Epithelial-Mesenchymal Transition

By E. Carver, R. Jiang, Y. Lan, Kathleen F. Oram, T. Gridley. Molecular and Cellular Biology, 2001

649 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/5e71b372e6fc7b2913723f17f0c6886a1d31c5f1

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Citations in the corpus

The transcriptional repressor Snail promotes mammary tumor recurrence. (2005, background): “First identified in Drosophila mutant embryos exhibiting defective mesoderm invagination, Snail is required for normal mesoderm development in mice (Grau et al., 1984; Carver et al., 2001).”
Differential expression of the epithelial-mesenchymal transition regulators snail, SIP1, and twist in gastric cancer. (2002, background): “One of the zinc finger proteins targeting these E-boxes is the transcription factor Snail which was shown to be a strong repressor of transcription of the E-cadherin gene.(7,13) Snail was found to evoke tumorigenic and invasive properties in epithelial cells on overexpression.”
Epithelial-mesenchymal transitions: insights from development (2012, background): “Snai1 knockout mice show a gastrulation phenotype, similar to that seen in Drosophila, suggesting a conserved role for Snai1 in EMT (Carver et al., 2001).”
Regulation of tight junctions during the epithelium-mesenchyme transition: direct repression of the gene expression of claudins/occludin by Snail (2003, background): “Furthermore, Snail-deficient mice died at the gastrulation stage because of incomplete EMT (Carver et al., 2001).”
Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease. (2009, positive): “Embryos lacking Snail activity fail to gastrulate, leading to an accumulation of epithelial cells still expressing E-cadherin that are unable to migrate (28, 29).”
Notch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformation. (2004, background): “This is consistent with the requirement for snail in the production of mesenchyme from epiblast cells during mouse gastrulation (Carver et al. 2001), and with the ability of snail to repress E-cadherin expression and induce EMT in epithelial tumor cells (Batlle et al. 2000; Cano et al. 2000).”
Targeted disruption of TGF-β1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction (2003, positive): “The Snail family of zinc-finger transcription factors are strong repressors of transcription of the E-cadherin gene and are implicated in both physiological and pathological EMT (18, 19, 33, 34).”
Snail Mediates E-Cadherin Repression by the Recruitment of the Sin3A/Histone Deacetylase 1 (HDAC1)/HDAC2 Complex (2004, background): “which maintains the expression of E-cadherin (12).”
TGF-β and epithelial-to-mesenchymal transitions (2005, background): “Snail represses transcription of the E-cadherin gene in cultured cells (Batlle et al., 2000; Cano et al., 2000) and during mesoderm formation in early embryonic development (Carver et al., 2001).”
Making a commitment: cell lineage allocation and axis patterning in the early mouse embryo (2009, background): “Snail-mutant embryos develop nascent mesoderm but these cells retain an epithelial morphology and fail to efficiently downregulate E-cadherin expressio”