Product Description
Size: 1Kit
SNAI1 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 5 bp deletion in exon2 and 68 bp insertion in exon2.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 5 bp deletion in exon2 and 68 bp insertion in exon2.,
Disease:Adenocarcinoma
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-SNAI1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
SNAIL also known as SNAI1 is a zinc finger transcription factor involved in the regulation of cellular processes. The SNAIL protein has a mass of approximately 29 kDa and is robustly expressed in various tissues including embryonic tissues and cancerous cells. The protein functions as a repressor of transcription influencing the expression of genes associated with cellular adhesion and movement. Due to its integral role SNAIL is involved in complex regulatory networks that control cell fate and differentiation.
Biological function summary
SNAIL contributes to the epithelial-mesenchymal transition (EMT) a process critical for embryogenesis and tumor progression. It forms a part of a complex network of transcription factors that regulate cell-cell adhesion molecules like E-cadherin. SNAIL's ability to bind to specific DNA sequences allows it to suppress or activate the transcription of target genes promoting cellular metamorphosis and enabling cells to acquire motility and invade other tissues.
Pathways
SNAIL operates significantly within the TGF-beta and Wnt signaling pathways. The TGF-beta pathway enhances the expression of SNAIL which in turn represses genes that maintain the epithelial phenotype. The Wnt pathway also modulates SNAIL activity connecting it with proteins such as beta-catenin to drive EMT. These pathways highlight SNAIL's involvement in sophisticated signaling pathways that determine cell behavior adaptation and tissue remodeling.
Overexpression of SNAIL associates with cancer progression particularly in metastasis due to its role in EMT. It connects with proteins like Slug and ZEB1 in this context enhancing the invasive capabilities of cancer cells. Moreover SNAIL is implicated in fibrotic diseases where excessive tissue scarring occurs. In such conditions TGF-beta-mediated activation of SNAIL contributes to abnormal tissue remodeling and fibrosis. The involvement of SNAIL in these diseases marks it as a potential target for therapeutic intervention.
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Collaboration
Tony Tang
Email: Tony.Tang@iright.com
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