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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Snail homolog 1

SNAIL, SNAI1, Snail1
The Drosophila embryonic protein snail is a zinc finger transcriptional repressor which downregulates the expression of ectodermal genes within the mesoderm. The nuclear protein encoded by this gene is structurally similar to the Drosophila snail protein, and is also thought to be critical for mesoderm formation in the developing embryo. At least two variants of a similar processed pseudogene have been found on chromosome 2. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: E-cadherin, Slug, CAN, ZEB1, vimentin
Papers on SNAIL
Tissue factor associates with survival and regulates tumour progression in osteosarcoma.
Versteeg et al., Leiden, Netherlands. In Thromb Haemost, Feb 2016
Tissue Factor was knocked down in 143B cells, which led to reduced expression of IL-8, CXCL-1, SNAIL and MMP2, but not MMP9.
Sprouty4 mediates amphiregulin-induced down-regulation of E-cadherin and cell invasion in human ovarian cancer cells.
Leung et al., Vancouver, Canada. In Tumour Biol, Feb 2016
In addition, we showed that small interfering RNA (siRNA)-mediated knockdown of SPRY4 attenuated the AREG-induced down-regulation of E-cadherin by inhibiting the expression of SNAIL but not SLUG.
Proteomic analysis of epithelial to mesenchymal transition reveals crosstalk between SNAIL and HDAC1 in breast cancer cells.
Faca et al., São Paulo, Brazil. In Mol Cell Proteomics, Feb 2016
Overexpression of transcription factors such as SNAIL, SLUG, ZEB1/2, and TWIST1, also induce EMT and are correlated to cancer aggressiveness.
Early Regulation of Profibrotic Genes in Primary Human Cardiac Myocytes by Trypanosoma cruzi.
Nde et al., Nashville, United States. In Plos Negl Trop Dis, Jan 2016
The transcriptome microarray data, validated by quantitative Real-Time PCR, was also confirmed by immunoblotting and customized Enzyme Linked Immunosorbent Assays (ELISA) array showing significant increases in the protein expression levels of fibrogenic EGR1, SNAI1 and IL 6.
The transcription factors Slug (SNAI2) and Snail (SNAI1) regulate phospholipase D (PLD) promoter in opposite ways towards cancer cell invasion.
Gomez-Cambronero et al., Dayton, United States. In Mol Oncol, Jan 2016
UNASSIGNED: Slug (SNAI2) and Snail (SNAI1) are master regulatory transcription factors for organogenesis and wound healing, and they are involved in the epithelial to mesenchymal transition (EMT) of cancer cells.
Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity.
Anastasiadis et al., Jacksonville, United States. In Nat Cell Biol, Sep 2015
PLEKHA7 regulates the levels of select miRNAs, in particular processing of miR-30b, to suppress expression of cell transforming markers promoted by the basolateral complex, including SNAI1, MYC and CCND1.
Metastatic pheochromocytoma and paraganglioma.
Kaltsas et al., Athens, Greece. In Eur J Clin Invest, Sep 2015
Plasma and urinary methoxytyramine are the biochemical markers characterizing metastatic PCs/PGLs along with evolving molecular markers such as miRNAs and SNAIL.
[SNAI1 and SNAI2 - transcriptional master-regulators of epithelial-mesenchimal transition].
Sverdlov et al., In Patol Fiziol Eksp Ter, Apr 2015
In this review we analyze molecular structure and mechanisms of regulation of two closely-related transcription factors SNAI1 and SNAI2, which play an important role in induction and progression of epithelial-mesenchymal transition during both normal development and carcinogenesis.
DEAR1, a novel tumor suppressor that regulates cell polarity and epithelial plasticity.
Killary et al., Houston, United States. In Cancer Res, 2014
DEAR1 binds to and promotes the ubiquitination of SMAD3, the major effector of TGFβ-mediated EMT, as well as downregulates SMAD3 targets SNAIL1/2, master transcriptional regulators of EMT.
PKD1 phosphorylation-dependent degradation of SNAIL by SCF-FBXO11 regulates epithelial-mesenchymal transition and metastasis.
Kang et al., Princeton, United States. In Cancer Cell, 2014
The transcription factor SNAIL promotes EMT and elicits associated pathological characteristics such as invasion, metastasis, and stemness.
Molecular mechanisms of epithelial-mesenchymal transition.
Derynck et al., San Francisco, United States. In Nat Rev Mol Cell Biol, 2014
This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels.
SLUG: Critical regulator of epithelial cell identity in breast development and cancer.
Kuperwasser et al., Boston, United States. In Cell Adh Migr, 2013
SLUG, a member of the SNAIL family of transcriptional repressors, is known to play a diverse number of roles in the cell, and its deregulation has been observed in a variety of cancers including breast.
Central role of Snail1 in the regulation of EMT and resistance in cancer: a target for therapeutic intervention.
Bonavida et al., In J Exp Clin Cancer Res, 2013
Snail1 is the founding member of the Snail superfamily of zinc-finger transcription factors, which also includes Snail2 (Slug) and Snail3 (Smuc).
The collagen receptor discoidin domain receptor 2 stabilizes SNAIL1 to facilitate breast cancer metastasis.
Longmore et al., Saint Louis, United States. In Nat Cell Biol, 2013
We show that activation of the collagen I receptor DDR2 (discoidin domain receptor 2) regulates SNAIL1 stability by stimulating ERK2 activity, in a Src-dependent manner.
Hyperglycemia causes renal cell damage via CCN2-induced activation of the TrkA receptor: implications for diabetic nephropathy.
Mason et al., London, United Kingdom. In Diabetes, 2012
hyperglycemia caused an induction of phosphorylated extracellular signal-related kinase 1/2 and Snail1 that was abrogated by silencing of TrkA or CCN2 using small interfering RNA
Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis.
Rudnicki et al., Ottawa, Canada. In Mol Cell, 2012
In primary myoblasts, snai1-HDAC1/2 repressive complex binds and excludes MyoD from its targets.
Canonical Wnt suppressor, Axin2, promotes colon carcinoma oncogenic activity.
Weiss et al., Ann Arbor, United States. In Proc Natl Acad Sci U S A, 2012
Axin2 acts as a potent promoter of carcinoma behavior by up-regulating the activity of the transcriptional repressor, Snail1, inducing a functional epithelial-mesenchymal transition (EMT) program and driving metastatic activity
Manganese superoxide dismutase induces migration and invasion of tongue squamous cell carcinoma via H2O2-dependent Snail signaling.
Zhou et al., Guangzhou, China. In Free Radic Biol Med, 2012
High snail1 is associated with migration and invasion of tongue squamous cell carcinoma.
[The role of transcription factor Snail1 in the regulation of hormonal sensitivity of in vitro cultured breast cancer cells].
Krasil'nikov et al., In Vopr Onkol, 2011
Decrease in the estrogen dependency of breast cancer cells is accompanied by an increase in Snail1 expression and activity, and demonstrated the Snail1 involvement in the negative regulation of ER.
A SNAIL1-SMAD3/4 transcriptional repressor complex promotes TGF-beta mediated epithelial-mesenchymal transition.
Fuxe et al., Stockholm, Sweden. In Nat Cell Biol, 2009
Data sugget that activation of a SNAIL1-SMAD3/4 transcriptional complex represents a mechanism of gene repression during EMT.
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