Snail family transcriptional repressor 1 (SNAIL) is a transcription factor and the gene encoding it is localized on human chromosome 20q13.13.
Immunogen
Peptide with sequence RKPSDPNRKPNY-C, from the N-terminal region of the protein sequence according to NP_005976.2
Biochem/physiol Actions
Snail family transcriptional repressor 1 (SNAIL) acts as a repressor of genes associated with the epithelial phenotype like E-cadherin and increases the expression of genes linked with the mesenchymal phenotype. It has a role in epithelial-mesenchymal transition. The protein aids in G1 transition (early to late) in the cell cycle. SNAIL also modulates cell-matrix adhesion.
Features and Benefits
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Physical form
Supplied at 0.5 mg/mL in 20mM Tris (pH 7.3) and 150mM NaCl with 0.02% sodium azide and 0.5% bovine serum albumin.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
CRISPR/Cas9n-Mediated Deletion of the Snail 1Gene (SNAI1) Reveals Its Role in Regulating Cell Morphology, Cell-Cell Interactions, and Gene Expression in Ovarian Cancer (RMG-1) Cells.
Haraguchi M
PLoS ONE (2015)
TP53 Mutation, Epithelial-Mesenchymal Transition, and StemlikeFeatures in Breast Cancer Subtypes
Danila Coradini
Journal of Biomedicine and Biotechnology (2012)
SNAIL transcription factor increases the motility and invasive capacity of prostate cancer cells.
Metformin is an inhibitor of oxidative phosphorylation that displays an array of anticancer activities. The interference of metformin with the activity of multi-drug resistance systems in cancer cells has been reported. However, the consequences of the acquired chemoresistance for the
International journal of molecular sciences, 22(8) (2021-05-01)
Glioblastoma multiforme (GBM) recurrences after temozolomide (TMZ) treatment result from the expansion of drug-resistant and potentially invasive GBM cells. This process is facilitated by O6-Methylguanine-DNA Methyltransferase (MGMT), which counteracts alkylating TMZ activity. We traced the expansion of invasive cell lineages
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