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Validated All-in-One™ qPCR Primer for SNAI2(NM_003068.4) Search again
Product ID:
HQP109945
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SLUG, SLUGH, SLUGH1, SNAIL2, WS2D
Gene Description:
snail family transcriptional repressor 2
Target Gene Accession:
NM_003068.4(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
This gene encodes a member of the Snail family of C2H2-type zinc finger transcription factors. The encoded protein acts as a transcriptional repressor that binds to E-box motifs and is also likely to repress E-cadherin transcription in breast carcinoma. This protein is involved in epithelial-mesenchymal transitions and has antiapoptotic activity. Mutations in this gene may be associated with sporatic cases of neural tube defects.
Gene References into function
- The SLUG zinc-finger protein represses E-cadherin in breast cancer.
- Absence of SLUG causes the auditory-pigmentary symptoms in at least some individuals with Wardenburg syndrome type 2.
- Results suggest that aberrant expression of Snail or Slug may promote tumorigenesis through increased resistance to programmed cell death.
- induction of Slug by autocrine production of SCF and c-Kit activation plays a key role in chemoresistance of malignant mesothelioma
- Tumors with positive Slug expression invaded deeper, had more lymph node metastasis, and had more lymphatic invasion than the tumors with negative Slug expression.
- SLUG is a negative regulator for BRCA2 gene expression
- SLUG levels in the cell regulated the function of cytokeratins 8 and 19 gene promoters.
- High levels of Snail predict decreased relapse-free survival in women with breast cancer.
- SLUG is upregulated by dihydrotestosterone and epidermal growth factor, providing a molecular mechanism by which epithelial cell-specific genes are silenced during prostate cancer development and progression.
- Slug regulates integrin alpha3, beta1, and beta4 expression and cell proliferation in human epidermal keratinocytes
- Slug overexpression may contribute to specific cardiac phenotypes and cancer development.
- These findings support a role of Slug in mediating Raf 1-induced transcriptional repression of occludin and subsequent epithelial to mesenchymal transition.
- Results suggest that the aryl hydrocarbon receptor participates in Slug induction, which, in turn, regulates cellular physiology including cell adhesion and migration.
- we provide evidence through yeast two-hybrid and in vitro co-immunoprecipitation analyses that hSLUG does not directly interact with hCtBP1.
- Data show that SNAI1 and SNAI2 are ectopically expressed in thyroid carcinomas, and aberrant expression in mice is associated with papillary carcinoma development.
- Ligand-induced Notch activation, through the induction of Slug, promotes tumor growth and metastasis characterized by epithelial-to-mesenchymal transition.
- Myocardin-related transcription factors are critical mediators of transforming growth factor beta (TGF-beta) 1-induced epithelial-mesenchymal transition.[
- Knockdown of SIM2s in MCF-7 breast cancer cells contributed to an epithelial-mesenchymal transition associated with increased slug levels.
- SLUG binds to the E2-box sequences of the VDR gene promoter and recruits CtBP1 and HDAC1, which results in the inhibition of VDR gene expression by chromatin remodeling.
- The effect of Etrogen receptor alpha on slug repression is dependent on the overall level of ERalpha, confirming that slug is an estrogen receptor alpha responsive gene.
- Slug down-regulation facilitates apoptosis induced by proapoptotic drugs in neuroblastoma cells and decreases their invasion capability in vitro and in vivo
- Collectively, our data suggest that combined expression of Slug and Snail is required for EMT in cardiac cushion morphogenesis.
- Slug is an essential component of the pathway leading to EGFR-mediated epithelial outgrowth
- These results implicate a novel EGFR/Erk5/Slug pathway in the control of cytoskeleton organization and cell motility in keratinocytes treated with epidermal growth factor.
- 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.
- SLUG-induced epithelial-mesenchymal transition may alter the expression profile of receptor tyrosine kinases, including discoid domain receptors
- Factors released by breast cancer cells are able to upregulate Slug expression in vascular endothelial cells.