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Validated All-in-One™ qPCR Primer for SNAI1(NM_005985.3) Search again
Product ID:
HQP110039
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SLUGH2, SNA, SNAH, SNAIL, SNAIL1, dJ710H13.1
Gene Description:
snail family transcriptional repressor 1
Target Gene Accession:
NM_005985.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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].
Gene References into function
- Snail expression inversely correlates with the grade of differentiation of the tumours and that it is expressed in all the infiltrating ductal carcinomas (IDC) presenting lymph node metastases that were analysed.
- SNA1 plays a role in repressing E-cadherin and MUC1 in epithelial cells
- Snail is a new inducer of MMP-2 expression which contributes to the increased invasion of squamous cell carcinoma cells
- E-cadherin and claudins/occludin have roles in the regulation of tight junctions during the epithelium-mesenchyme transition, but are repressed by snail
- Hypoxia induces down-regulation of E-cadherin in ovarian carcinoma cells, via up-regulation of the transcriptional repressor SNAIL.
- Snail expression may be induced during hepatocellular cell carcinoma progression; Snail directly represses gene transcription and activates invasion via upregulation of MMP gene family
- Results indicate that Snail is involved in both the direct transcriptional repression of genes and post-transcriptional.These data support the idea that Snail is a transcription factor possessing pleiotropic activities.
- Snail transcription is driven by signaling pathways known to induce epithelial to mesenchymal transition, reinforcing the role of Snail in this proces
- Results suggest that aberrant expression of Snail or Slug may promote tumorigenesis through increased resistance to programmed cell death.
- SNAl1 is regulated by GSK-3beta-mediated phosphorylation in control of epithelial-mesenchymal transition.
- E-cadherin mRNA expression in synovial sarcoma was associated with reduced Snail expression level
- Data show that the activity of glycogen synthase kinase-3 (GSK-3) is necessary for the maintenance of the epithelial architecture, and that GSK-3 inhibition stimulates the transcription of Snail.
- Wnt signaling stabilizes Snail and beta-catenin proteins in tandem fashion so as to cooperatively engage transcriptional programs that control an epithelial-mesenchymal transition.
- demonstrated, for the first time, that SNAIL is upregulated in colon cancer, which potentially may have significance in control of metastasis and possibly serve as a target for chemopreventive agents
- Over expression of Smad-interacting protein 1 is associated with ovarian carcinoma aggressiveness
- zinc finger domain functions as a nuclear localization signal, can be transported into the nucleus by importin beta-mediated
- Snail may play a role in recurrence by downregulating E-cadherin and inducing an epithelial-to-mesenchymal transition in breast cancer.
- SNAIL expression in colorectal tumors is associated with downregulation of E-cadherin (CDH1) and vitamin D receptor gene products
- Human cancers that overexpress snail may have a survival advantage to genotoxic and potentially other forms of stress
- The pattern of Snail expression suggests only a minor role of Snail in tumours of the upper gastrointestinal tract.
- Snail is present in activated mesenchymal cells indicating its relevance in the communication between tumor and stroma and suggest that it can promote the conversion of carcinoma cells to stromal cells.
- These findings indicate that Snail upregulation by HGF is mediated via the MAPK/Egr-1 signaling pathway and that both Snail and Egr-1 play a critical role in HGF-induced cell scattering, migration, and invasion.
- These results indicate that NBS1 overexpression induces EMT through the upregulation of Snail expression, and co-expression of NBS1/Snail predicts metastasis in HNSCCs
- VHL promotes E2 box-dependent E-cadherin transcription by HIF-mediated regulation of SIP1 and snail
- The identification of a beta-catenin-T-cell factor-regulated Axin2-GSK3beta-Snail1 axis provides new mechanistic insights into cancer-associated epithelial-mesenchymal transition programmes.
- Overexpression of a constitutively activated IGF-IR (CD8-IGF-IR) was sufficient to cause transformation of immortalized human mammary epithelial cells and growth in immunocompromised mice.
- the Snail promoter is constitutively packaged in a poised chromatin structure that can be activated in melanoma cells by a tissue-specific enhancer, which physically contacts the promoter
- Snail1 is involved in renal tubular EMT and TGF-beta1 regulates Snail1 at the transcription and protein degradation levels
- Data show that SNAI1 and SNAI2 are ectopically expressed in thyroid carcinomas, and aberrant expression in mice is associated with papillary carcinoma development.
- Snail and SHH are overexpressed in a large subset of NETs of the ileum.
- RKIP is a novel component of the Snail transcriptional regulatory network important for the progression and metastasis of cancer.
- Snail is associated with lower overall survival of ovarian cancer patients.
- These data are in line with a proposed role for Snail in endometrial tumor progression.
- Analysis of cell lines derived from lymph node metastasis indicates that SNAI1 expression is required for metastatic dissemination.
- These data show that Snail functions as a molecular mediator of TGF-beta1-regulated MMP-9 expression by increasing Ets-1 and thereby contributing to oral cancer progression.
- These results lead to a new hypothesis that Snail and ZEB1 are downstream of CCN6 and play a critical role in CCN6-mediated regulation of E-cadherin in breast cancer.
- A positive feedback stimulation of the Wnt pathway by activation of snail.
- A novel autocrine function for VEGF in breast tumor cells in driving the expression of Snail, a breast tumor progression factor.
- Overexpression of Snail is associated with up-regulation of proinflammatory mediators and inhibits differentiation in oral keratinocytes and thus head and neck squamous cell carcinomas
- EGF cooperates with alpha(5)beta(1) integrin signaling to induce EMT in cervical cancer cells via up-regulated Snail
- These results suggest that bile acids repress E-cadherin through the induction of transcription factor Snail
- Snail and Slug promote formation of beta-catenin-T-cell factor (TCF)-4 transcription complexes that bind to the promoter of the TGF-beta3 gene to increase its transcription.
- HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression.
- class I histone deacetylase (HDACs), specifically HDAC2, and the transcriptional repressor Snail play a central role in the suppression of 15-hydroxyprostaglandin dehydrogenase expression.
- Factors released by breast cancer cells are able to upregulate Snail expression in vascular endothelial cells.
- The Snail-p53 binding as the new therapeutic target for K-Ras-mutated cancers including pancreatic, lung, and colon cancers.
- Snail1-mediated suppression of CYLD plays a key role in melanoma malignancy.