Dual regulation of Snail by GSK-3β-mediated phosphorylation in control of epithelial–mesenchymal transition

By Binhua P. Zhou, Jiong Deng, W. Xia, Jihong Xu, Y. Li, M. Gunduz, M. Hung. Nature Cell Biology, 2004

1,679 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/e4a02e7e42ad6e6c04a03705e5f5ae21a9f75921

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Citations in the corpus

• The many faces and functions of β‐catenin (2012, unknown): “GSK3 b normally phosphorylates Snail1 and marks it for degradation (Zhou et al , 2004; Yook et al , 2006).”
• Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript In particular, TWIST-induced suppression of E cadherin transcription is indirect and mediated by its transcriptional activation of SNAI2, as SNAI2 knockdown blocks the ability of TWIST to activate EMT in mammary cells (C”
• New signals from the invasive front (2006, background): “It is rapidly phosphorylated by glycogen synthase kinase-3β (GSK-3β) and subsequently degraded by the ubiquitin–proteasome pathwa”
• Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. (2008, background): “Hence, inactivation of GSK3b via the Wnt pathway or receptor tyrosine kinases may promote Snail stability and nuclear import, thus activating its ability to promote EMT (Bachelder et al., 2005; Zhou et al., 2004).”
• Experimental adaptation of an influenza H5 haemagglutinin (HA) confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferrets (2012, methodology): “Because GSK3! phosphorylates SNAI, which leads to ubiquitination and proteasomal degradation (13), we investigated whether STAT3 is involved in the ubiquitin-mediated proteasomal degradation of SNAI via GSK3!.”
• Epithelial–mesenchymal transition in tumor metastasis (2016, background): “Ubiquitin-mediated proteasome degradation of SNAIL1 and TWIST1 after GSK3b or MAP kinase phosphorylation is another mechanism of EMT-TF modulation (Hong et al., 2011; Zhou et al., 2004).”
• Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “…al. 2000; Cano et al. 2000; Hajra et al. 2002), promoter methylation (Graff et al. 1995; Kanai et al. 1997; Saito et al. 1998), and protein phosphorylation and degradation (Zhou et al. 2004; Bachelder et al. 2005; Lester et al. 2007) have all been observed in response to various inducing signals.”
• Dynamic EMT: a multi‐tool for tumor progression (2021, unknown): “Intracellularly, the WNT-induced block of GSK 3 b is not only promoting b -catenin cytoplasmic accumulation, but also stabilizes SNAIL (Zhou et al , 2004 ).”
• Epithelial-mesenchymal transitions: insights from development (2012, background): “Snail is phosphorylated by Pak1 (Pak – FlyBase) and glycogen synthase kinase 3 (GSK3) for activation and downregulation, respectively (Zhou et al., 2004; Yang et al., 2005).”
• The Role of Snail in EMT and Tumorigenesis (2013, background): “Glycogen synthase kinase-3β (GSK-3β) is the major kinase responsible for the phosphorylation at the SRD region [20,21]; whereas small C-terminal domain phosphatase (SCP) interacts with Snail and removes these phosphorylations [22].”