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Human Polyclonal SNAI1 Primary Antibody pour IF, IHC (p) - ABIN498268
Feng, Di, Tao, Chang, Lu, Fan, Shan, Li, Yang: PDK1 regulates vascular remodeling and promotes epithelial-mesenchymal transition in cardiac development. dans Molecular and cellular biology 2010
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Guinea Pig Polyclonal SNAI1 Primary Antibody pour IHC, WB - ABIN2777858
Zhou, Deng, Xia, Xu, Li, Gunduz, Hung: Dual regulation of Snail by GSK-3beta-mediated phosphorylation in control of epithelial-mesenchymal transition. dans Nature cell biology 2004
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Human Monoclonal SNAI1 Primary Antibody pour IHC, WB - ABIN2668578
Rosivatz, Becker, Kremmer, Schott, Blechschmidt, Höfler, Sarbia: Expression and nuclear localization of Snail, an E-cadherin repressor, in adenocarcinomas of the upper gastrointestinal tract. dans Virchows Archiv : an international journal of pathology 2006
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Human Monoclonal SNAI1 Primary Antibody pour ELISA, WB - ABIN969409
Wanami, Chen, Peiró, García de Herreros, Bachelder: Vascular endothelial growth factor-A stimulates Snail expression in breast tumor cells: implications for tumor progression. dans Experimental cell research 2008
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Human Polyclonal SNAI1 Primary Antibody pour FACS, ICC - ABIN4899437
Satelli, Mitra, Brownlee, Xia, Bellister, Overman, Kopetz, Ellis, Meng, Li: Epithelial-mesenchymal transitioned circulating tumor cells capture for detecting tumor progression. dans Clinical cancer research : an official journal of the American Association for Cancer Research 2015
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Human Polyclonal SNAI1 Primary Antibody pour WB - ABIN388812
Barbu, Zhang, Berenstein, Groves, Parks, Siraganian: The transcription factor Zeb2 regulates signaling in mast cells. dans Journal of immunology (Baltimore, Md. : 1950) 2012
Human Monoclonal SNAI1 Primary Antibody pour IHC, WB - ABIN2452265
Qin, He, Tang, Ye, Dang, Lu, Wang, Li, Yan, Ma: MicroRNAs Provide Feedback Regulation of Epithelial-Mesenchymal Transition Induced by Growth Factors. dans Journal of cellular physiology 2015
Human Monoclonal SNAI1 Primary Antibody pour IF, ELISA - ABIN520326
Rath, Miller, Litofsky, Anthony, Feng, Franklin, Pei, Free, Liu, Ren, Kirk, Shi: Isolation and characterization of a population of stem-like progenitor cells from an atypical meningioma. dans Experimental and molecular pathology 2011
Human Monoclonal SNAI1 Primary Antibody pour ELISA, WB - ABIN967055
Herranz, Pasini, Díaz, Francí, Gutierrez, Dave, Escrivà, Hernandez-Muñoz, Di Croce, Helin, García de Herreros, Peiró: Polycomb complex 2 is required for E-cadherin repression by the Snail1 transcription factor. dans Molecular and cellular biology 2008
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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 (Montrer CDH1 Anticorps) 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 (Montrer CISH Anticorps)-regulatory modules in native conformation are critical for Drosophila snail expression.
The Snail repressor positions Notch (Montrer NOTCH1 Anticorps) signaling in the Drosophila embryo.
results show that Sna has a positive regulatory function on sim (Montrer SIM2 Anticorps) expression in the presumptive mesectoderm; this positive effect of Sna depends on the Su(H (Montrer RBPJ Anticorps))-binding sites within the sim (Montrer SIM2 Anticorps) promoter, suggesting that Sna regulates Notch (Montrer NOTCH1 Anticorps) 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 (Montrer PCDH8 Anticorps)) to promote tissue separation through novel functions.
Interaction with Snail1/2, and Twist function more generally, is regulated by GSK-3-beta (Montrer GSK3b Anticorps)-mediated phosphorylation of conserved sites in the WR domain.
the same E3 ubiquitin ligase (Montrer MUL1 Anticorps) known to regulate Snail family proteins, Partner of paired (Ppa (Montrer FBXL14 Anticorps)), also controlled Twist stability and did so in a manner dependent on the Twist WR-rich domain
Low glucose culture hampered typical epithelial-mesenchymal transition-like morphological change, "cadherin switching," and cell migration of hepatocellular carcinoma cells through inducing persistent down-regulation of HSF1 (Montrer HSF1 Anticorps), resulting in direct inhibition of snail1 expression.
A20 (Montrer TNFAIP3 Anticorps) promotes metastasis of aggressive basal-like breast cancers through multi-monoubiquitylation of Snail1.
Results indicate that the increase of snail protein expression may play an important role in the carcinogenesis, progression, and metastasis of gastric cancer.
Study provides evidence that SNAI1 promotes renal cell carcinoma (Montrer MOK Anticorps) migration and invasion. Its expression is regulated by miR (Montrer MLXIP Anticorps)-211 which targets its 3'-UTR (Montrer UTS2R Anticorps).
FLNA (Montrer FLNA Anticorps) upregulation correlates with Snail-induced epithelial to mesenchymal transition in colorectal carcinoma.
Slug (Montrer SNAI2 Anticorps) is a positive regulator, and Snail a negative regulator, of PLD2 (Montrer PLD2 Anticorps) expression.
Metagenomic analysis revealed direct correlation between PPARGC1A (Montrer PPARGC1A Anticorps), SNAI1, and metastatic lung disease.
Results indicate that HCV core induced epithelial-mesenchymal transition (EMT (Montrer ITK Anticorps)) by interacting with the transcriptional repressor complex Snail/HDAC1 (Montrer HDAC1 Anticorps)/2 at the E-cadherin (Montrer CDH1 Anticorps) promoter, which led to E-cadherin (Montrer CDH1 Anticorps) repression and increased invasiveness of hepatoma cells.
High SNAIL expression is associated with liver neoplasms.
Results demonstrated that over expression of Snail suppresses Cryptic expression and confirmed that Snail directly binds to Cryptic gene promoter and regulates its expression.
both Snail and Slug (Montrer SNAI2 Anticorps) are able to form binary complexes with either YAP (Montrer YAP1 Anticorps) or TAZ (Montrer TAZ Anticorps) that, together, control YAP (Montrer YAP1 Anticorps)/TAZ (Montrer TAZ Anticorps) transcriptional activity and function throughout mouse development.
results demonstrate that skeletal stem/stromal cell mobilize Snail/Slug (Montrer SNAI2 Anticorps)-YAP (Montrer YAP1 Anticorps)/TAZ (Montrer TAZ Anticorps) complexes to control stem cell function
these results might suggest that calcineurin inhibitor (Montrer RCAN1 Anticorps)-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 (Montrer TP53 Anticorps) in breast cancer
Snail1 deficiency modified the phenotype of pancreatic tumors .
miR (Montrer MLXIP Anticorps)-200 promotes the mesenchymal to epithelial transition by suppressing multiple members of the Zeb2 (Montrer ZEB2 Anticorps) and Snail1 transcriptional repressor complexes, such as Smad2 (Montrer SMAD2 Anticorps) and Smad5 (Montrer SMAD5 Anticorps).
show that Snail1-induced fibrosis can be reversed in vivo and that obstructive nephropathy can be therapeutically ameliorated in mice by targeting Snail1 expression
Results suggest that Snai1 is a key factor that triggers ESCs (Montrer NR2E3 Anticorps) exit from the pluripotency state and initiate their differentiation processes.
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