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Disruption of Snail expression in follicle stem cells compromises proliferation, but not maintenance. FSCs with excessive Snail expression had increased proliferation and lifespan, accompanied by a moderate decrease inE-cadherin expression (required for adhesion of FSCs to their niche) at the junction between their adjacent cells, indicating a conserved role of Snail in E-cadherin (show CDH1 Proteins) inhibition.
during gastrulation of Drosophila embryos, Sna expression downregulates polarity protein Baz which in turn results in junction disassembly at protein levels.
evidence for mechanosensitivity of cell-cell junctions and implications that myosin-mediated tension can prevent Snail-driven Eepithelial-mesenchymal transitions
Snail can potentiate enhancer activation by collaborating with different activators, providing a new mechanism by which Snail regulates development.
Rapid transcription kinetics and negative autoregulation are responsible for the remarkable homogeneity of snail expression and the coordination of mesoderm invagination.
Study shows that Sna represses transcription of pbl in the mesoderm primordium of D. melanogaster via one or more Sna-binding sites, which are conserved among species of the Drosophila genus, but not in the mosquito, correlating with the different modes of gastrulation in the different genuses.
Complex interactions between cis (show CISH Proteins)-regulatory modules in native conformation are critical for Drosophila snail expression.
The Snail repressor positions Notch (show NOTCH1 Proteins) signaling in the Drosophila embryo.
results show that Sna has a positive regulatory function on sim (show SIM2 Proteins) expression in the presumptive mesectoderm; this positive effect of Sna depends on the Su(H (show RBPJ Proteins))-binding sites within the sim (show SIM2 Proteins) promoter, suggesting that Sna regulates Notch (show NOTCH1 Proteins) signaling
snail is required for Drosophila gastrulation and is not replaceable by Escargot or Worniu.
The transcription factor Snail1 is essential for tissue separation, enabling paraxial protocadherin (PAPC (show PCDH8 Proteins)) to promote tissue separation through novel functions.
Interaction with Snail1/2, and Twist function more generally, is regulated by GSK-3-beta-mediated phosphorylation of conserved sites in the WR domain.
the same E3 ubiquitin ligase (show MUL1 Proteins) known to regulate Snail family proteins, Partner of paired (Ppa (show FBXL14 Proteins)), also controlled Twist stability and did so in a manner dependent on the Twist WR-rich domain
our results suggest that Cx32 (show GJB1 Proteins) inhibits Hepatocellular carcinoma (HCC (show FAM126A Proteins)) invasion and metastasis through Snail-mediated EMT (show ITK Proteins), Cx32 (show GJB1 Proteins) and this signaling pathway molecules may offer potential targets for HCC (show FAM126A Proteins) cancer therapy
The data suggest that reduced expression of E-cadherin (show CDH1 Proteins) and over-expression of Slug, Snail, and TGF-beta (show TGFB1 Proteins) induce epithelial to mesenchymal transition in ameloblastoma.
this study shows that during epithelial-mesenchymal transition in the prostate cancer cell line RbBP5 (show RBBP5 Proteins) binding is increased in the vicinity of Snail transcription start site
RND3 (show RND3 Proteins) promotes Snail 1 protein degradation in glioblastoma tumor cells, promoting cell migration and neoplasm invasiveness.
this study shows that EGF (show EGF Proteins) induces epithelial-mesenchymal transition through phospho-Smad2 (show SMAD2 Proteins)/3-Snail signaling pathway in breast cancer cells
SNAI1 is a direct and functional target of miR (show MLXIP Proteins)-182. However SNAI1 negatively regulates the expression of miR (show MLXIP Proteins)-182 in breast cancer cells.
E-cadherin (show CDH1 Proteins) expression was increased by transfection of p300 (show EP300 Proteins) small interfering RNA in a dose-dependent manner.. There was a correlation between Snail and p300 (show EP300 Proteins) expressions in lung cancer. Moreover, p300 (show EP300 Proteins) acetylates Snail both in vivo and in vitro, and K187 may be involved in this modification.
PARP3 (show PARP3 Proteins) controls of TGFbeta (show TGFB1 Proteins)-induced epithelial mesenchymal transformation and acquisition of stem-like cell features by stimulation transglutaminase 2 (show TGM2 Proteins)/SNAI1 signaling.
Results show that Snai1 binds to the PXDN (show PXDN Proteins) promoter in response to TGF-beta1 (show TGFB1 Proteins) treatment of cervical carcinoma cell lines and represses its expression.
increased Snail expression during progression to metastatic disease may prime cells for resistance to AR-targeted therapies by promoting AR activity in prostate cancer
a Snail1-ATGL (show PNPLA2 Proteins) axis that regulates adipose lipolysis and fatty acid release, is reported.
A20 (show TNFAIP3 Proteins) promotes metastasis of aggressive basal-like breast cancers through multi-monoubiquitylation of Snail1.
Metagenomic analysis revealed direct correlation between PPARGC1A, SNAI1, and metastatic lung disease.
both Snail and Slug are able to form binary complexes with either YAP (show YAP1 Proteins) or TAZ (show TAZ Proteins) that, together, control YAP (show YAP1 Proteins)/TAZ (show TAZ Proteins) transcriptional activity and function throughout mouse development.
results demonstrate that skeletal stem/stromal cell mobilize Snail/Slug-YAP (show YAP1 Proteins)/TAZ (show TAZ Proteins) complexes to control stem cell function
these results might suggest that calcineurin inhibitor (show RCAN1 Proteins)-induced tubular SNAI1 protein cytoplasmic accumulation, possibly because of impaired SNAI1 proteasomal degradation and nuclear translocation, might be a sign of a diseased profibrotic epithelial phenotype.
Snail1 as a molecular bypass that suppresses the anti-proliferative and pro-apoptotic effects exerted by wild-type p53 (show TP53 Proteins) in breast cancer
Snail1 deficiency modified the phenotype of pancreatic tumors .
miR (show MLXIP Proteins)-200 promotes the mesenchymal to epithelial transition by suppressing multiple members of the Zeb2 and Snail1 transcriptional repressor complexes, such as Smad2 (show SMAD2 Proteins) and Smad5 (show SMAD5 Proteins).
show that Snail1-induced fibrosis can be reversed in vivo and that obstructive nephropathy can be therapeutically ameliorated in mice by targeting Snail1 expression
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.
snail homolog 1
, snail like protein
, Protein snail-like protein 1
, snail homolog 1 (Drosophila)
, snail 1 homolog
, zinc-finger transcription factor Snail
, protein Xsnail
, protein snail homolog Sna
, protein xSna
, snail protein
, zinc finger protein with snail domain similar to escargot
, transcription factor protein
, snail zinc finger protein
, snail-like protein 1
, protein sna
, protein snail homolog 1
, snail 1 zinc finger protein
, snail 1, zinc finger protein
, zinc finger protein SNAI1